Journal of Hainan Medical University
Volume ,2026 Issue 12
indexed by
- Featured Articles
- Recommended Topics
-
- Exploring the protective effects and mechanisms of Daphniphyllum calycinum‑Polygonum hydropiper on gastric mucosal injury based on network pharmacology and experimental verification
- Spatial‑temporal clustering of tuberculosis in Hainan Island from 2018 to 2022
- To optimize the salt process of Amomum longiligulare T.L.Wu based on entropy weight method combined with response surface method
- Network pharmacology research and experimental verification of Li Medicine Nauclea officinalis in the treatment of diabetic nephropathy
- The pyroptosis mechanism of pectic polysaccharides of Rauvolfia erticillata(Lour.) Baill.var. hainanensis Tsiang in regulating ulcerative colitis mice through MAPK/NF‑κB signaling pathway
-
Journal of Hainan Medical University has been consecutively listed in Chinese Core Journals (Source Journal for Chinese Scientific and Technical Papers and Citations)
Dr. Dirk Engels (Former Director of Control of Neglected Tropical Diseases of WHO) joined HMU Press for academic exchanges
Strengthening academic achievement with SCI-indexed Journals，building a platform for international exchanges
Professor Jong-Yil Chai (Seoul University, Korea) come to visit our university
Professor Michele Samaja of the University of Milan, Italy, came to our university for an exchange visit
Professor Adrin Angel Inchauspe, National University of La Plata, Argentina, made an academic visit to our journal
Professor Marcel Tanner, President of Swiss Academy of Natural Sciences, visited our university with Dr. Dirk Engels, Director of the Department of Prevention and Control of Neglected Tropical Diseases of the World Health Organization
- Current Issue
- Online First
- Archive
- Most Downloaded
Select AllDeselectExport
Display Method:
2026(12):881-889, DOI: 10.13210/j.cnki.jhmu.20250314.001
Abstract:
Objective:To investigate the role and mechanism of γδT cells regulating the transforming growth factor‑β （TGF‑β）/Smad signaling pathway through interleukin‑17 （IL‑17） in intestinal fibrosis， based on the Crohn's disease （CD） intestinal fibrosis model. Methods:A total of twenty‑eight male BALB/c mice were randomly picked out. Thereafter， these mice were classified into four separate groups： the control group， the model group， the anti‑IL‑17A antibody intervention group， and the anti‑TCR γ/δ antibody intervention group. Construct a CD intestinal fibrosis model using TNBS/50% alcohol enema and inject corresponding antibodies. Record the weight and disease activity index （DAI） of mice， and after euthanizing the mice in the 7th week， take colon tissue and measure its length. H&E staining was used to observe changes in tissue morphology and structure； Masson staining was used to observe collagen in colon tissue； Immunohistochemical detection of the expression of α‑smooth muscle actin （α‑SMA）； ELISA was used to detect the expression levels of IL‑17， TGF‑β， interferon‑γ （IFN‑γ）， and IL‑10； Western blot was used to detect α‑SMA， connective tissue growth factor （CTGF）， type Ⅰ collagen （Collagen Ⅰ）， Collagen Ⅲ， and TGF‑β/Smad signaling pathway related proteins. Results:Compared to the control group， the model group showed an increase in DAI score and a reduction in colon length； Pathological examination showed severe damage to the colon tissue， and Masson staining revealed a large number of blue stained collagen fibers； The expression of IFN‑γ and IL‑10 decreased， while the expression of IL‑17， TGF‑β， α‑SMA， CTGF， Collagen Ⅰ， Collagen Ⅲ， TGF‑β1， Smad2/3， and p‑Smad2/3 showed a significant increase （P<0.05）. However， in comparison to the model group， treatment with anti‑IL‑17A antibody or anti TCR γ/δ antibody significantly inhibited the changes in various indicators induced by TNBS in mice （P<0.05） and alleviated intestinal fibrosis. Conclusion:Gamma delta T cells can promote intestinal fibrosis， and the mechanism of action may be related to the activation of the IL‑17 signaling pathway.
Objective:To investigate the role and mechanism of γδT cells regulating the transforming growth factor‑β （TGF‑β）/Smad signaling pathway through interleukin‑17 （IL‑17） in intestinal fibrosis， based on the Crohn's disease （CD） intestinal fibrosis model. Methods:A total of twenty‑eight male BALB/c mice were randomly picked out. Thereafter， these mice were classified into four separate groups： the control group， the model group， the anti‑IL‑17A antibody intervention group， and the anti‑TCR γ/δ antibody intervention group. Construct a CD intestinal fibrosis model using TNBS/50% alcohol enema and inject corresponding antibodies. Record the weight and disease activity index （DAI） of mice， and after euthanizing the mice in the 7th week， take colon tissue and measure its length. H&E staining was used to observe changes in tissue morphology and structure； Masson staining was used to observe collagen in colon tissue； Immunohistochemical detection of the expression of α‑smooth muscle actin （α‑SMA）； ELISA was used to detect the expression levels of IL‑17， TGF‑β， interferon‑γ （IFN‑γ）， and IL‑10； Western blot was used to detect α‑SMA， connective tissue growth factor （CTGF）， type Ⅰ collagen （Collagen Ⅰ）， Collagen Ⅲ， and TGF‑β/Smad signaling pathway related proteins. Results:Compared to the control group， the model group showed an increase in DAI score and a reduction in colon length； Pathological examination showed severe damage to the colon tissue， and Masson staining revealed a large number of blue stained collagen fibers； The expression of IFN‑γ and IL‑10 decreased， while the expression of IL‑17， TGF‑β， α‑SMA， CTGF， Collagen Ⅰ， Collagen Ⅲ， TGF‑β1， Smad2/3， and p‑Smad2/3 showed a significant increase （P<0.05）. However， in comparison to the model group， treatment with anti‑IL‑17A antibody or anti TCR γ/δ antibody significantly inhibited the changes in various indicators induced by TNBS in mice （P<0.05） and alleviated intestinal fibrosis. Conclusion:Gamma delta T cells can promote intestinal fibrosis， and the mechanism of action may be related to the activation of the IL‑17 signaling pathway.
2026(12):890-899, DOI: 10.13210/j.cnki.jhmu.20250306.003
Abstract:
Objective:To investigate the neurotoxic effects of CdCl2 exposure during pregnancy and lactation on hippocampal injury in offspring mice. Methods:The pregnant mice were divided into 3 groups： the control group， the 5 mg/kg group and the 10 mg/kg CdCl2 group. The pregnant and lactating mice were respectively administered intragastrically with normal saline， 5 mg/kg and 10 mg/kg of CdCl2. The birth status， physical development， histopathological changes and hippocampal cell apoptosis of offspring mice were observed. The brain organ coefficient was calculated. ICP⁃MS was used to evaluate the changes in cadmium， zinc and iron levels in the brain and blood of PDN1 and PDN30 offspring. qRT⁃PCR was used to analyze the expression of inflammatory neurological function⁃related factors in the hippocampus of PND1 and PND30 offspring. Results:CdCl2 exposure during pregnancy and lactation had no effect on the body weight of PND1， PND30 offspring mice and maternal mice. The brain organ coefficient of PND1 offspring in the 10 mg/kg group was reduced （P<0.01）. CdCl2 exposure will lead to increased PND1 offspring's brain cadmium， and PND30 offspring's brain or blood cadmium， decreased iron and zinc levels （P<0.05）. On the 2nd， 3rd， 4th and 5th days of positioning navigation， the escape latency of PND30 offspring in the 5 mg/kg and 10 mg/kg groups was prolonged compared to the control group （P<0.01）； The spatial exploration test data showed that the times of the PND30 offspring in the 5 mg/kg and 10 mg/kg groups crossed the platform， and the target quadrant residence time was reduced （P<0.05）. CdCl2 exposure caused different degrees of pathological changes in the CA1 and CA3 regions of the hippocampus of PND30 offspring mice， increased apoptosis in the CA1 and DG regions， and no pathological changes were found in the hippocampus of PND1 offspring. Compared to the control group， the mRNA of IL⁃1β， IL⁃6， TNF⁃α， APP， Tau， Ki67， BDNF， GFAP， Nestin， Arg⁃1， IL⁃4， and IL⁃10 in the 5mg/kg and 10mg/kg groups did not show statistically significant differences in the brain of the PND1 offspring（P>0.05）； The mRNA expression of IL⁃1β， IL⁃6， TNF⁃α， APP， and Tau was upregulated in the 5 mg/kg or 10 mg/kg groups， and the expression of IL⁃4， IL⁃10， Arg⁃1， Ki67， BDNF， GFAP， and Nestin was downregulated in the hippocampus of the PND30 offspring mice （P<0.05）. Conclusion:CdCl2 exposure during pregnancy or lactation proves that a small amount of CdCl2 enters the offspring through the placental glucocorticoid barrier and the blood⁃brain barrier， and most of it is transferred to the offspring through breast milk， which can cause reduced iron and zinc levels in PND1 and PND30 offspring， as well as damage to hippocampal memory and neurological function in PND30 offspring， and induce brain inflammatory response.
Objective:To investigate the neurotoxic effects of CdCl2 exposure during pregnancy and lactation on hippocampal injury in offspring mice. Methods:The pregnant mice were divided into 3 groups： the control group， the 5 mg/kg group and the 10 mg/kg CdCl2 group. The pregnant and lactating mice were respectively administered intragastrically with normal saline， 5 mg/kg and 10 mg/kg of CdCl2. The birth status， physical development， histopathological changes and hippocampal cell apoptosis of offspring mice were observed. The brain organ coefficient was calculated. ICP⁃MS was used to evaluate the changes in cadmium， zinc and iron levels in the brain and blood of PDN1 and PDN30 offspring. qRT⁃PCR was used to analyze the expression of inflammatory neurological function⁃related factors in the hippocampus of PND1 and PND30 offspring. Results:CdCl2 exposure during pregnancy and lactation had no effect on the body weight of PND1， PND30 offspring mice and maternal mice. The brain organ coefficient of PND1 offspring in the 10 mg/kg group was reduced （P<0.01）. CdCl2 exposure will lead to increased PND1 offspring's brain cadmium， and PND30 offspring's brain or blood cadmium， decreased iron and zinc levels （P<0.05）. On the 2nd， 3rd， 4th and 5th days of positioning navigation， the escape latency of PND30 offspring in the 5 mg/kg and 10 mg/kg groups was prolonged compared to the control group （P<0.01）； The spatial exploration test data showed that the times of the PND30 offspring in the 5 mg/kg and 10 mg/kg groups crossed the platform， and the target quadrant residence time was reduced （P<0.05）. CdCl2 exposure caused different degrees of pathological changes in the CA1 and CA3 regions of the hippocampus of PND30 offspring mice， increased apoptosis in the CA1 and DG regions， and no pathological changes were found in the hippocampus of PND1 offspring. Compared to the control group， the mRNA of IL⁃1β， IL⁃6， TNF⁃α， APP， Tau， Ki67， BDNF， GFAP， Nestin， Arg⁃1， IL⁃4， and IL⁃10 in the 5mg/kg and 10mg/kg groups did not show statistically significant differences in the brain of the PND1 offspring（P>0.05）； The mRNA expression of IL⁃1β， IL⁃6， TNF⁃α， APP， and Tau was upregulated in the 5 mg/kg or 10 mg/kg groups， and the expression of IL⁃4， IL⁃10， Arg⁃1， Ki67， BDNF， GFAP， and Nestin was downregulated in the hippocampus of the PND30 offspring mice （P<0.05）. Conclusion:CdCl2 exposure during pregnancy or lactation proves that a small amount of CdCl2 enters the offspring through the placental glucocorticoid barrier and the blood⁃brain barrier， and most of it is transferred to the offspring through breast milk， which can cause reduced iron and zinc levels in PND1 and PND30 offspring， as well as damage to hippocampal memory and neurological function in PND30 offspring， and induce brain inflammatory response.
2026(12):900-907, DOI: 10.13210/j.cnki.jhmu.20250314.006
Abstract:
Objective:To investigate the risk factors for early neurological deterioration （END） in patients with acute ischemic stroke with TOAST classification of large artery atherosclerosis （LAA）， and to establish a nomogram prediction model and evaluate it. Methods:Consecutive patients with large‑artery atherosclerotic acute ischemic stroke （LAA‑AIS） who were hospitalized in our hospital between October 2023 and September 2024 were included. Patients were categorized into END and non‑END groups based on an increase of ≥2 points in the total NIHSS score or an increase of ≥1 point in the score of motor function within 7 d after onset. SPSS27.0 was applied to perform univariate analysis， and binary Logistic regression analysis was used for variables with P<0.05 to screen out the independent risk factors for END in LAA‑AIS patients， a nomogram prediction model was constructed. The ROC curve and its area under the curve （AUC） value were used to assess the differentiation of the model， the calibration curve was used to assess the accuracy of the model， and the decision curve analysis （DCA） was used to assess the clinical utility of the model. Results:A total of 249 patients with LAA‑AIS were included， including 190 （76.3%） males and 59 （23.7%） females， aged 63 （53，73） years； 62 （24.9%） in the END group and 187 （75.1%） in the non‑END group. Univariate analysis found 6 variables to be statistically different （P<0.05）， and 4 variables were screened out by including them in binary Logistic regression analysis： BMI （OR=1.171， 95%CI 1.032 to 1.329， P=0.015）， systolic blood pressure at admission （OR=1.015， 95%CI 1.001 to 1.030， P=0.030）， glycosylated hemoglobin （OR=1.286， 95%CI 1.064 to 1.555， P=0.009）， and low‑density lipoprotein cholesterol （LDL‑C） （OR=2.278， 95%CI 1.272 to 4.079， P=0.006） were the independent risk factors for the development of END in LAA‑AIS patients. A nomogram prediction model was constructed based on the above 4 factors， and internal validation was performed using the Bootstrap method to draw ROC curves， calibration curves， and DCA curves. The results showed that the AUC of the model was 0.735； the calibration plot predicted values were in good agreement with the actual values， and the DCA curve showed that the prediction model had high clinical utility. Conclusion:Elevated LDL cholesterol， systolic blood pressure on admission， BMI， and glycosylated hemoglobin levels are independent risk factors for the development of END in patients with LAA‑AIS， and the column‑line graphic prediction model based on them is a reliable and easy‑to‑use tool for predicting the development of END in patients with LAA‑AIS.
Objective:To investigate the risk factors for early neurological deterioration （END） in patients with acute ischemic stroke with TOAST classification of large artery atherosclerosis （LAA）， and to establish a nomogram prediction model and evaluate it. Methods:Consecutive patients with large‑artery atherosclerotic acute ischemic stroke （LAA‑AIS） who were hospitalized in our hospital between October 2023 and September 2024 were included. Patients were categorized into END and non‑END groups based on an increase of ≥2 points in the total NIHSS score or an increase of ≥1 point in the score of motor function within 7 d after onset. SPSS27.0 was applied to perform univariate analysis， and binary Logistic regression analysis was used for variables with P<0.05 to screen out the independent risk factors for END in LAA‑AIS patients， a nomogram prediction model was constructed. The ROC curve and its area under the curve （AUC） value were used to assess the differentiation of the model， the calibration curve was used to assess the accuracy of the model， and the decision curve analysis （DCA） was used to assess the clinical utility of the model. Results:A total of 249 patients with LAA‑AIS were included， including 190 （76.3%） males and 59 （23.7%） females， aged 63 （53，73） years； 62 （24.9%） in the END group and 187 （75.1%） in the non‑END group. Univariate analysis found 6 variables to be statistically different （P<0.05）， and 4 variables were screened out by including them in binary Logistic regression analysis： BMI （OR=1.171， 95%CI 1.032 to 1.329， P=0.015）， systolic blood pressure at admission （OR=1.015， 95%CI 1.001 to 1.030， P=0.030）， glycosylated hemoglobin （OR=1.286， 95%CI 1.064 to 1.555， P=0.009）， and low‑density lipoprotein cholesterol （LDL‑C） （OR=2.278， 95%CI 1.272 to 4.079， P=0.006） were the independent risk factors for the development of END in LAA‑AIS patients. A nomogram prediction model was constructed based on the above 4 factors， and internal validation was performed using the Bootstrap method to draw ROC curves， calibration curves， and DCA curves. The results showed that the AUC of the model was 0.735； the calibration plot predicted values were in good agreement with the actual values， and the DCA curve showed that the prediction model had high clinical utility. Conclusion:Elevated LDL cholesterol， systolic blood pressure on admission， BMI， and glycosylated hemoglobin levels are independent risk factors for the development of END in patients with LAA‑AIS， and the column‑line graphic prediction model based on them is a reliable and easy‑to‑use tool for predicting the development of END in patients with LAA‑AIS.
2026(12):908-916, DOI: 10.13210/j.cnki.jhmu.20260515.001
Abstract:
Objective:To investigate the expression characteristics of paraspinal muscle‑derived osteonectin in adolescent idiopathic scoliosis （AIS） and its effect on osteogenic differentiation， providing evidence for elucidating aberrant myokine regulation of paraspinal muscles in AIS.: Methods:Multiplex immunoassays were used to measure multiple myokines levels in peripheral blood and the concave and convex sides of apical vertebra paraspinal muscle of the control and AIS patients. Immunohistochemistry and qPCR were used to assess protein and mRNA expressions of osteonectin in bilateral paraspinal muscles. An in vitro muscle‑bone co‑culture model was established using human skeletal muscle myoblasts （HSMM） infected with lentivirus to overexpress osteonectin and induce myotube differentiation. After collecting the culture medium supernatant， conditioned medium from osteonectin‑overexpressing cells （OE‑CM group） and regular HSMM‑conditioned medium （CM group） were prepared to culture primary AIS osteoblasts. The effects of osteonectin on osteogenic differentiation were evaluated by alkaline phosphatase （ALP） staining and qPCR. Results:The results of multiplex immunoassays indicated that the levels of osteonectin， fatty acid‑binding protein 3， and erythropoietin in the peripheral blood of the AIS patients were significantly decreased compared to the controls （P<0.05）. Immunohistochemistry revealed a reduced expression of osteonectin protein in AIS paraspinal muscles， with lower expression on the concave side than the convex side （P<0.01）. qPCR and multiplex immunoassays confirmed that the osteonectin mRNA and protein expressions were lower on the concave side than the convex side （P<0.05）. The ALP positive staining of primary AIS osteoblasts was significantly enhanced in the OE‑CM group compared to the CM group， and qPCR showed that the mRNA levels of ALP， RUNX2， and COL1A1 in osteoblasts of the OE‑CM group were significantly upregulated （P<0.001）. Conclusion:AIS patients exhibit abnormal expression of multiple myokines in peripheral blood and imbalanced secretory function of the concave and convex sides of paraspinal muscle. Osteonectin promotes osteogenic differentiation of primary AIS osteoblasts by enhancing ALP activity and upregulating osteogenic gene expressions， suggesting that osteonectin‑mediated myokine regulation may contribute to the pathogenesis and progression of AIS through modulating bone metabolism.
Objective:To investigate the expression characteristics of paraspinal muscle‑derived osteonectin in adolescent idiopathic scoliosis （AIS） and its effect on osteogenic differentiation， providing evidence for elucidating aberrant myokine regulation of paraspinal muscles in AIS.: Methods:Multiplex immunoassays were used to measure multiple myokines levels in peripheral blood and the concave and convex sides of apical vertebra paraspinal muscle of the control and AIS patients. Immunohistochemistry and qPCR were used to assess protein and mRNA expressions of osteonectin in bilateral paraspinal muscles. An in vitro muscle‑bone co‑culture model was established using human skeletal muscle myoblasts （HSMM） infected with lentivirus to overexpress osteonectin and induce myotube differentiation. After collecting the culture medium supernatant， conditioned medium from osteonectin‑overexpressing cells （OE‑CM group） and regular HSMM‑conditioned medium （CM group） were prepared to culture primary AIS osteoblasts. The effects of osteonectin on osteogenic differentiation were evaluated by alkaline phosphatase （ALP） staining and qPCR. Results:The results of multiplex immunoassays indicated that the levels of osteonectin， fatty acid‑binding protein 3， and erythropoietin in the peripheral blood of the AIS patients were significantly decreased compared to the controls （P<0.05）. Immunohistochemistry revealed a reduced expression of osteonectin protein in AIS paraspinal muscles， with lower expression on the concave side than the convex side （P<0.01）. qPCR and multiplex immunoassays confirmed that the osteonectin mRNA and protein expressions were lower on the concave side than the convex side （P<0.05）. The ALP positive staining of primary AIS osteoblasts was significantly enhanced in the OE‑CM group compared to the CM group， and qPCR showed that the mRNA levels of ALP， RUNX2， and COL1A1 in osteoblasts of the OE‑CM group were significantly upregulated （P<0.001）. Conclusion:AIS patients exhibit abnormal expression of multiple myokines in peripheral blood and imbalanced secretory function of the concave and convex sides of paraspinal muscle. Osteonectin promotes osteogenic differentiation of primary AIS osteoblasts by enhancing ALP activity and upregulating osteogenic gene expressions， suggesting that osteonectin‑mediated myokine regulation may contribute to the pathogenesis and progression of AIS through modulating bone metabolism.
2026(12):917-924, DOI: 10.13210/j.cnki.jhmu.20250307.001
Abstract:
Objective:To investigate the specific mechanism of how Erdong Xiaoke Decoction （EDXKD） regulates lacrimal gland autophagy through the phosphatidylinositol 3‑kinase（PI3K）/protein kinase B（AKT）/mammalian target of rapamycin（mTOR） pathway， thereby improving the dry eye condition in diabetes rats. Methods:A total of 20 healthy male SD rats were randomly divided into the control group， the model group， the traditional Chinese medicine（TCM）group， and the prophylactic drug group， with 5 rats in each group. The rats in the control group were fed with standard diet， and the rats in the other groups were fed with high sugar and fat diet. After 4 weeks， streptozotocin （STZ） was injected intraperitoneally for 8 consecutive weeks to establish the model of type 2 diabetes dry eye rats. The control group and the model group were given 10 mL/kg physiological saline by gavage， the TCM group was given 11 g/kg EDXKD by gavage， and the prophylactic drug group was given sodium hyaluronate eye drops in both eyes for 4 consecutive weeks. Before modeling， after modeling， and after intervention， dry eye related indicators such as corneal fluorescence staining （FL）， tear film rupture time （BUT）， and phenol red cotton thread test （PRT） were compared in each group of rats. After sampling， the weight of the lacrimal gland was measured， and H&E staining was used for pathological observation of the lacrimal gland. Transmission electron microscopy was used to observe autophagosomes in the lacrimal gland. And Western blot and RT‑PCR techniques were used to detect the expression of PI3K， AKT， mTOR， microtubule associated protein 1 light chain 3 （LC3）， chelator‑1 （SQSTM1/p62） protein and mRNA in the lacrimal gland. Results:After modeling， there was no statistically significant difference in dry eye indicators among all groups except the control group （P>0.05）. Compared to the control group， the other groups showed an increase in FL and a decrease in BUT and PRT （P<0.05）. After intervention， compared to the control group， the model group rats showed significant dry eye symptoms， with an increase in FL， a decrease in BUT and PRT（P<0.05）， a reduction in lacrimal gland weight（P<0.05）， atrophy of H&E stained glandular lobules， dilation of glandular lumen， a decrease in autophagosomes under electron microscopy， and activation of PI3K， AKT， mTOR phosphorylation and increased mRNA expression in lacrimal gland tissue（P<0.05）. Compared to the model group， both the TCM group and the prophylactic drug group showed a reversal of the above indicators（P<0.05）. Conclusion:EDXKD inhibits the activation of PI3K/AKT/mTOR pathway in lacrimal gland of diabetes dry eye rats， and increases autophagy level to alleviate lacrimal gland damage， thereby alleviating dry eye symptoms.
Objective:To investigate the specific mechanism of how Erdong Xiaoke Decoction （EDXKD） regulates lacrimal gland autophagy through the phosphatidylinositol 3‑kinase（PI3K）/protein kinase B（AKT）/mammalian target of rapamycin（mTOR） pathway， thereby improving the dry eye condition in diabetes rats. Methods:A total of 20 healthy male SD rats were randomly divided into the control group， the model group， the traditional Chinese medicine（TCM）group， and the prophylactic drug group， with 5 rats in each group. The rats in the control group were fed with standard diet， and the rats in the other groups were fed with high sugar and fat diet. After 4 weeks， streptozotocin （STZ） was injected intraperitoneally for 8 consecutive weeks to establish the model of type 2 diabetes dry eye rats. The control group and the model group were given 10 mL/kg physiological saline by gavage， the TCM group was given 11 g/kg EDXKD by gavage， and the prophylactic drug group was given sodium hyaluronate eye drops in both eyes for 4 consecutive weeks. Before modeling， after modeling， and after intervention， dry eye related indicators such as corneal fluorescence staining （FL）， tear film rupture time （BUT）， and phenol red cotton thread test （PRT） were compared in each group of rats. After sampling， the weight of the lacrimal gland was measured， and H&E staining was used for pathological observation of the lacrimal gland. Transmission electron microscopy was used to observe autophagosomes in the lacrimal gland. And Western blot and RT‑PCR techniques were used to detect the expression of PI3K， AKT， mTOR， microtubule associated protein 1 light chain 3 （LC3）， chelator‑1 （SQSTM1/p62） protein and mRNA in the lacrimal gland. Results:After modeling， there was no statistically significant difference in dry eye indicators among all groups except the control group （P>0.05）. Compared to the control group， the other groups showed an increase in FL and a decrease in BUT and PRT （P<0.05）. After intervention， compared to the control group， the model group rats showed significant dry eye symptoms， with an increase in FL， a decrease in BUT and PRT（P<0.05）， a reduction in lacrimal gland weight（P<0.05）， atrophy of H&E stained glandular lobules， dilation of glandular lumen， a decrease in autophagosomes under electron microscopy， and activation of PI3K， AKT， mTOR phosphorylation and increased mRNA expression in lacrimal gland tissue（P<0.05）. Compared to the model group， both the TCM group and the prophylactic drug group showed a reversal of the above indicators（P<0.05）. Conclusion:EDXKD inhibits the activation of PI3K/AKT/mTOR pathway in lacrimal gland of diabetes dry eye rats， and increases autophagy level to alleviate lacrimal gland damage， thereby alleviating dry eye symptoms.
2026(12):925-935, DOI: 10.13210/j.cnki.jhmu.20250328.001
Abstract:
Objective:To investigate the potential targets and mechanisms of action of Danggui Buxue Decoction （DGBXD） for the treatment of diabetic osteoporosis （DOP） based on network pharmacology， molecular docking， and animal experiments. Methods:The active chemical components of DGBXD were screened by a network pharmacology approach to retrieve the targets of DGBXD related to diabetes osteoporosis. Protein‑protein interaction （PPI） networks of drug‑disease targets were constructed. Validate the interactions between major targets and active chemical components by molecular docking. Using a db/db diabetic mouse model， the potential targets of DGBXD intervention in DOP were validated and the mechanism of action was explored by ELISA， Western blot and pathology. Results:A total of 413 targets for the action of Astragalus and 65 targets for the action of Angelica sinensis were obtained by network pharmacology， and 15 330 genes were retrieved as DOP‑related disease targets. The total number of targets of DGBXD for DOP was 202， including 190 from Astragalus and 11 from Angelica sinensis. Network pharmacological enrichment analysis indicated that DGBXD may improve osteogenic abnormalities in DOP by regulating inflammatory factor expression through modulating TNF‑α expression and PI3K‑AKT signaling pathway. The results of animal experiments showed that compared to the control group， the serum IL‑6， IL‑8 and TNF‑α levels were significantly increased in the model group （P<0.05）； the intervention of DGBXD could inhibit the excessive IL‑6 （P<0.05），IL‑8 （P<0.05） and TNF‑α （P<0.05） expressions in the model group. Pathological results showed that DGBXD could correct the disorders of bone formation caused by abnormal inflammatory response. Western blot results further indicated that compared to the model group， the intervention of DGBXD could significantly reduce the protein expression of TNF‑α， AKT， phosphorylated AKT， and correct the abnormal protein expression of BMP2 （P<0.05）. Conclusion:DGBXD may inhibit the inflammatory response and enhance the expression of BMP2 by regulating the TNF‑α/PI3K‑AKT/BMP signaling pathway， thus promoting the synthesis and mineralization of bone matrix， alleviating the high glucose‑induced osteogenic inhibition， improving the balance of bone metabolism， and achieving the therapeutic effect on DOP.
Objective:To investigate the potential targets and mechanisms of action of Danggui Buxue Decoction （DGBXD） for the treatment of diabetic osteoporosis （DOP） based on network pharmacology， molecular docking， and animal experiments. Methods:The active chemical components of DGBXD were screened by a network pharmacology approach to retrieve the targets of DGBXD related to diabetes osteoporosis. Protein‑protein interaction （PPI） networks of drug‑disease targets were constructed. Validate the interactions between major targets and active chemical components by molecular docking. Using a db/db diabetic mouse model， the potential targets of DGBXD intervention in DOP were validated and the mechanism of action was explored by ELISA， Western blot and pathology. Results:A total of 413 targets for the action of Astragalus and 65 targets for the action of Angelica sinensis were obtained by network pharmacology， and 15 330 genes were retrieved as DOP‑related disease targets. The total number of targets of DGBXD for DOP was 202， including 190 from Astragalus and 11 from Angelica sinensis. Network pharmacological enrichment analysis indicated that DGBXD may improve osteogenic abnormalities in DOP by regulating inflammatory factor expression through modulating TNF‑α expression and PI3K‑AKT signaling pathway. The results of animal experiments showed that compared to the control group， the serum IL‑6， IL‑8 and TNF‑α levels were significantly increased in the model group （P<0.05）； the intervention of DGBXD could inhibit the excessive IL‑6 （P<0.05），IL‑8 （P<0.05） and TNF‑α （P<0.05） expressions in the model group. Pathological results showed that DGBXD could correct the disorders of bone formation caused by abnormal inflammatory response. Western blot results further indicated that compared to the model group， the intervention of DGBXD could significantly reduce the protein expression of TNF‑α， AKT， phosphorylated AKT， and correct the abnormal protein expression of BMP2 （P<0.05）. Conclusion:DGBXD may inhibit the inflammatory response and enhance the expression of BMP2 by regulating the TNF‑α/PI3K‑AKT/BMP signaling pathway， thus promoting the synthesis and mineralization of bone matrix， alleviating the high glucose‑induced osteogenic inhibition， improving the balance of bone metabolism， and achieving the therapeutic effect on DOP.
2026(12):936-946, DOI: 10.13210/j.cnki.jhmu.20250314.004
Abstract:
Objective:To investigate the mechanism of action of Huanglian Jiedu Decoction in the treatment of type 2 diabetes mellitus by network pharmacology and 16S rRNA sequencing methods. Methods:The active ingredients and targets of Huanglian Jiedu Decoction were screened in the TCM Systematic Pharmacology Database and Analysis Platform （TCMSP）， and the obtained targets were imported into the protein database （UniProt） to find the corresponding gene names. Disease targets were collected in the human genome database （GeneCards）， the online human Mendelian genetic database （OMIM）， and the TTD database. The intersection targets of drugs and diseases were obtained through the Venn diagram， and the "drug ingredient‑disease target" network was constructed by using Cytoscape 3.7.2 software to determine the key active ingredients. Protein‑protein interaction （PPI） analysis was performed through the STRING database， and key targets were screened using the plug‑in function in Cytoscape 3.7.2 software. Then， the KEGG enrichment analysis was carried out through the Metascape database， and the "drug component‑disease target‑signaling pathway" network was constructed to identify the key signaling pathways. Finally， the network pharmacology results were verified by H&E staining and 16S rRNA sequencing. Results:A total of 85 active ingredients and 236 corresponding targets were found in Huanglian Jiedu Decoction， and 1 549 disease targets were found by network pharmacology analysis. There were 133 intersecting targets and 62 corresponding active ingredients. The key active ingredients in Huanglian Jiedu Decoction are quercetin and wogonin， etc. The core targets of the PPI network analysis were protein kinase 1 （AKT1）， tumor necrosis factor （TNF）， interleukin‑6 （IL‑6）， and phosphoinositide 3‑kinase / protein kinase B （PI3K/ Akt） signaling pathways are closely related. Through animal experiments， it was found that compared to the normal group， the colon tissue structure of the rats in the model group was abnormal， the glands were atrophied and disordered， the spacing between some glands was widened， and the goblet cells were significantly reduced. After the intervention of Huanglian Jiedu Decoction， the tissue structure of the colon was significantly improved， the glands were arranged neatly， and a large number of goblet cells could be seen. In addition， Huanglian Jiedu Decoction could affect the richness and diversity of intestinal microbiota， increasing the abundance of Firmicutes at the phylum level， decreasing the abundance of Bacteroides， and increasing the abundance of beneficial bacteria such as Lactobacillus， Allobaculum and Blautia at the genus level. LEfSe analysis showed that Allobaculum， Lactococcus and Blautia were differential markers in the treatment of type 2 diabetes mellitus by Huanglian Jiedu Decoction. Conclusion:Huanglian Jiedu Decoction can promote the proliferation of beneficial bacteria， reduce intestinal inflammation， and repair the intestinal barrier to treat type 2 diabetes.
Objective:To investigate the mechanism of action of Huanglian Jiedu Decoction in the treatment of type 2 diabetes mellitus by network pharmacology and 16S rRNA sequencing methods. Methods:The active ingredients and targets of Huanglian Jiedu Decoction were screened in the TCM Systematic Pharmacology Database and Analysis Platform （TCMSP）， and the obtained targets were imported into the protein database （UniProt） to find the corresponding gene names. Disease targets were collected in the human genome database （GeneCards）， the online human Mendelian genetic database （OMIM）， and the TTD database. The intersection targets of drugs and diseases were obtained through the Venn diagram， and the "drug ingredient‑disease target" network was constructed by using Cytoscape 3.7.2 software to determine the key active ingredients. Protein‑protein interaction （PPI） analysis was performed through the STRING database， and key targets were screened using the plug‑in function in Cytoscape 3.7.2 software. Then， the KEGG enrichment analysis was carried out through the Metascape database， and the "drug component‑disease target‑signaling pathway" network was constructed to identify the key signaling pathways. Finally， the network pharmacology results were verified by H&E staining and 16S rRNA sequencing. Results:A total of 85 active ingredients and 236 corresponding targets were found in Huanglian Jiedu Decoction， and 1 549 disease targets were found by network pharmacology analysis. There were 133 intersecting targets and 62 corresponding active ingredients. The key active ingredients in Huanglian Jiedu Decoction are quercetin and wogonin， etc. The core targets of the PPI network analysis were protein kinase 1 （AKT1）， tumor necrosis factor （TNF）， interleukin‑6 （IL‑6）， and phosphoinositide 3‑kinase / protein kinase B （PI3K/ Akt） signaling pathways are closely related. Through animal experiments， it was found that compared to the normal group， the colon tissue structure of the rats in the model group was abnormal， the glands were atrophied and disordered， the spacing between some glands was widened， and the goblet cells were significantly reduced. After the intervention of Huanglian Jiedu Decoction， the tissue structure of the colon was significantly improved， the glands were arranged neatly， and a large number of goblet cells could be seen. In addition， Huanglian Jiedu Decoction could affect the richness and diversity of intestinal microbiota， increasing the abundance of Firmicutes at the phylum level， decreasing the abundance of Bacteroides， and increasing the abundance of beneficial bacteria such as Lactobacillus， Allobaculum and Blautia at the genus level. LEfSe analysis showed that Allobaculum， Lactococcus and Blautia were differential markers in the treatment of type 2 diabetes mellitus by Huanglian Jiedu Decoction. Conclusion:Huanglian Jiedu Decoction can promote the proliferation of beneficial bacteria， reduce intestinal inflammation， and repair the intestinal barrier to treat type 2 diabetes.
2026(12):947-960, DOI: 10.13210/j.cnki.jhmu.20250917.002
Abstract:
Circulating tumor cell （CTC） and their clustered structure （CTC cluster） play a pivotal role in the process of distant tumor metastasis. However， they are extremely low abundance in peripheral blood， structural fragility， and phenotypic heterogeneity pose significant challenges for efficient detection via liquid biopsy. Achieving high⁃efficiency and structure⁃preserving enrichment of CTC and CTC cluster has become a critical technical bottleneck in the development of clinically applicable liquid biopsy systems. In recent years， various separation strategies have been proposed to address the phenotypic diversity and structural integrity of CTC and CTC cluster， including approaches based on physical properties， biomarker recognition， and integrated multi⁃modal techniques such as immunomagnetic beads， density gradient centrifugation， microfluidic chips， and functionalized nanoplatforms. This review systematically outlines the developmental trajectory of current mainstream enrichment technologies， with a focus on comparing their performance in terms of capture efficiency， structural preservation， throughput capacity， and clinical applicability. Special attention is given to their effectiveness in identifying low⁃expression heterogeneous subpopulations and preserving the intact architecture of CTC clusters. Furthermore， the review explores recent advancements involving novel materials and intelligent release mechanisms， highlighting the challenges and opportunities in functional research and clinical translation. The aim is to provide a comprehensive technical reference and theoretical foundation for building sensitive， specific， and practically applicable platforms for the detection of CTC and CTC cluster.
Circulating tumor cell （CTC） and their clustered structure （CTC cluster） play a pivotal role in the process of distant tumor metastasis. However， they are extremely low abundance in peripheral blood， structural fragility， and phenotypic heterogeneity pose significant challenges for efficient detection via liquid biopsy. Achieving high⁃efficiency and structure⁃preserving enrichment of CTC and CTC cluster has become a critical technical bottleneck in the development of clinically applicable liquid biopsy systems. In recent years， various separation strategies have been proposed to address the phenotypic diversity and structural integrity of CTC and CTC cluster， including approaches based on physical properties， biomarker recognition， and integrated multi⁃modal techniques such as immunomagnetic beads， density gradient centrifugation， microfluidic chips， and functionalized nanoplatforms. This review systematically outlines the developmental trajectory of current mainstream enrichment technologies， with a focus on comparing their performance in terms of capture efficiency， structural preservation， throughput capacity， and clinical applicability. Special attention is given to their effectiveness in identifying low⁃expression heterogeneous subpopulations and preserving the intact architecture of CTC clusters. Furthermore， the review explores recent advancements involving novel materials and intelligent release mechanisms， highlighting the challenges and opportunities in functional research and clinical translation. The aim is to provide a comprehensive technical reference and theoretical foundation for building sensitive， specific， and practically applicable platforms for the detection of CTC and CTC cluster.
Select AllDeselectExport
Display Method:
Select AllDeselectExport
Display Method:
2021,27(13):1036-1040, DOI: 10.13210/j.cnki.jhmu.20200706.001
Abstract:
Hepatic fibrosis is a common pathological basis for all chronic liver diseases， and a necessary stage for the progression of chronic liver disease into cirrhosis. Since various cells and cytokines， as pathogenic factors， play a major role in hepatic fibrosis， the pathogenesis of hepatic fibrosis is extremely complicated. This review focuses on the role of different cells and cytokines （macrophages， natural killer cells and natural killer T cells， tumor necrosis factor， IL-22， transforming growth factor beta， connective tissue growth factor， vascular endothelial growth factor） in the progression of hepatic fibrosis.
Hepatic fibrosis is a common pathological basis for all chronic liver diseases， and a necessary stage for the progression of chronic liver disease into cirrhosis. Since various cells and cytokines， as pathogenic factors， play a major role in hepatic fibrosis， the pathogenesis of hepatic fibrosis is extremely complicated. This review focuses on the role of different cells and cytokines （macrophages， natural killer cells and natural killer T cells， tumor necrosis factor， IL-22， transforming growth factor beta， connective tissue growth factor， vascular endothelial growth factor） in the progression of hepatic fibrosis.
2021,27(21):1672-1676, DOI: 10.13210/j.cnki.jhmu.20200904.005
Abstract:
Parkinson's disease （PD） is a neurodegenerative disorder due to gradual loss of dopaminergic neurons in the substantia nigra in the midbrain， however， the pathogenesis is unclear. There is a correlation between the excitability of striatal neurons and PD. Ion channels are important to maintain membrane potential and regulate excitability of neurons， but ionic mechanisms for modulation of neurons excitability are not fully understood. This article reviews the relationship between ion channels and excitability of striatal neurons in PD and ion channel changes in the pathogenesis of PD， in order to find new targets to treatment PD by intervening ion channels.
Parkinson's disease （PD） is a neurodegenerative disorder due to gradual loss of dopaminergic neurons in the substantia nigra in the midbrain， however， the pathogenesis is unclear. There is a correlation between the excitability of striatal neurons and PD. Ion channels are important to maintain membrane potential and regulate excitability of neurons， but ionic mechanisms for modulation of neurons excitability are not fully understood. This article reviews the relationship between ion channels and excitability of striatal neurons in PD and ion channel changes in the pathogenesis of PD， in order to find new targets to treatment PD by intervening ion channels.
2021,27(17):1350-1354, DOI: 10.13210/j.cnki.jhmu.20200814.002
Abstract:
Cytokines play an important role in the pathological process of atherosclerosis （AS）， affecting the progression and prognosis of AS-related cerebrovascular diseases. Cytokines mainly include C-reactive protein， interleukin， tumor necrosis factor， chemotactic cytokines， matrix metalloproteinases， etc. These cytokines promote or inhibit the inflammatory response and plaque formation during AS process through different targets and mechanisms. A comprehensive understanding of the cytokines in the occurrence and development of AS is conducive to search for new therapeutic targets and drugs.
Cytokines play an important role in the pathological process of atherosclerosis （AS）， affecting the progression and prognosis of AS-related cerebrovascular diseases. Cytokines mainly include C-reactive protein， interleukin， tumor necrosis factor， chemotactic cytokines， matrix metalloproteinases， etc. These cytokines promote or inhibit the inflammatory response and plaque formation during AS process through different targets and mechanisms. A comprehensive understanding of the cytokines in the occurrence and development of AS is conducive to search for new therapeutic targets and drugs.
2021,27(17):1307-1311, DOI: 10.13210/j.cnki.jhmu.20200715.005
Abstract:
Objective： To explore the expression and prognostic significance of ADHs in hepatocellular carcinoma （HCC）.Methods： The clinical data in this study were retrieved from The Cancer Genome Atlas （TCGA）. The expression of ADHs was differentially analyzed in normal liver tissues and HCC by using the Metabolic gEne RApid Visualizer and the TCGA database， and the differentially expressed ADHs were selected for Kaplan‑Meier survival analysis. Cox analysis was performed to select factors that may influence the prognosis of HCC and to verify independent risk factors for HCC patients. The interaction among ADHs was explored at the gene level and protein expression level through GeneMAMIA and STRING， and the functional enrichment analysis of ADH family was carried out by using DAVID bioinformatics resources. Results： The expression levels of ADH1A， ADH1B， ADH1C， ADH4 and ADH7 in HCC were low. Patients with low expression level of ADH1A， ADH1B， ADH1C and ADH4 had poor survival rates， which may be related to the poor prognosis of HCC. Univariate Cox regression analysis showed that the expression levels of ADH1A， ADH1C and ADH4， as well as the clinical stage， T stage and M stage of the tumor were closely related to the overall survival rate of the patients. Multivariate Cox regression analysis further suggested that the low expression of ADH1A， ADH1C and ADH4 were independent risk factors affecting the prognosis of HCC patients. There was a pathway between ADH1A‑ADH1B， ADH1B‑ADH1C and ADH1A‑ADH1C， and ADHs were closely related to esterase D and aldehyde dehydrogenase. The ADHs were mainly involved in biological processes such as ethanol oxidation and retinol metabolism， and played a biological role in glycolysis/gluconeogenesis， chemical carcinogenesis and metabolism of xenobiotics by cytochrome P450. Conclusion： ADH1A， ADH1C and ADH4 may be biomarkers for the prognosis of HCC， providing reference value for the practical application of ADHs in HCC.
Objective： To explore the expression and prognostic significance of ADHs in hepatocellular carcinoma （HCC）.Methods： The clinical data in this study were retrieved from The Cancer Genome Atlas （TCGA）. The expression of ADHs was differentially analyzed in normal liver tissues and HCC by using the Metabolic gEne RApid Visualizer and the TCGA database， and the differentially expressed ADHs were selected for Kaplan‑Meier survival analysis. Cox analysis was performed to select factors that may influence the prognosis of HCC and to verify independent risk factors for HCC patients. The interaction among ADHs was explored at the gene level and protein expression level through GeneMAMIA and STRING， and the functional enrichment analysis of ADH family was carried out by using DAVID bioinformatics resources. Results： The expression levels of ADH1A， ADH1B， ADH1C， ADH4 and ADH7 in HCC were low. Patients with low expression level of ADH1A， ADH1B， ADH1C and ADH4 had poor survival rates， which may be related to the poor prognosis of HCC. Univariate Cox regression analysis showed that the expression levels of ADH1A， ADH1C and ADH4， as well as the clinical stage， T stage and M stage of the tumor were closely related to the overall survival rate of the patients. Multivariate Cox regression analysis further suggested that the low expression of ADH1A， ADH1C and ADH4 were independent risk factors affecting the prognosis of HCC patients. There was a pathway between ADH1A‑ADH1B， ADH1B‑ADH1C and ADH1A‑ADH1C， and ADHs were closely related to esterase D and aldehyde dehydrogenase. The ADHs were mainly involved in biological processes such as ethanol oxidation and retinol metabolism， and played a biological role in glycolysis/gluconeogenesis， chemical carcinogenesis and metabolism of xenobiotics by cytochrome P450. Conclusion： ADH1A， ADH1C and ADH4 may be biomarkers for the prognosis of HCC， providing reference value for the practical application of ADHs in HCC.
2021,27(17):1281-1284, DOI: 10.13210/j.cnki.jhmu.20210716.002
Abstract:
The outbreak of COVID‑19 caused by severe acute respiratory syndrome coronavirus type 2 （SARS‑CoV‑2） in 2019 threatens global public health. In the early stage， respiratory symptoms are the most common in patients with new coronal pneumonia， but with the spread of the disease around the world， gastrointestinal symptoms such as diarrhea， nausea and vomiting have attracted more and more attention. And some patients take diarrhea as the first symptom， which is easy to cause missed diagnosis. This paper expounds the close relationship between COVID‑19 and gastrointestinal tract， and reviews the research progress of COVID‑19's effect on gastrointestinal tract.
The outbreak of COVID‑19 caused by severe acute respiratory syndrome coronavirus type 2 （SARS‑CoV‑2） in 2019 threatens global public health. In the early stage， respiratory symptoms are the most common in patients with new coronal pneumonia， but with the spread of the disease around the world， gastrointestinal symptoms such as diarrhea， nausea and vomiting have attracted more and more attention. And some patients take diarrhea as the first symptom， which is easy to cause missed diagnosis. This paper expounds the close relationship between COVID‑19 and gastrointestinal tract， and reviews the research progress of COVID‑19's effect on gastrointestinal tract.
LI Peng?yu, CUI Fu?yan, HUANG Jin?yue, TANG Meng, JIANG Jia?xin, MA Ying, XIA Nian?tong, YANG Bo, WANG Zhi?gang
2023,29(6):22-27, DOI: 10.13210/j.cnki.jhmu.20230217.001
Abstract:
Objective： A chiral resolution method for enantiomers of two chiral nitrogen⁃containing metabolites R⁃gentiandiol and S⁃gentiandiol of swertiamarin in plasma was developed， and the pharmacokinetics of the metabolites were studied. Methods： The metabolites of swertiamarin in vivo were detected by LC⁃MS/MS using Astec Cyclobond Ⅱ Cyclodextrin column （4.6 mm×100 mm， 5 μm）， gradient elution with acetonitrile⁃water as mobile phase， and monitored by multiple reaction monitoring （MRM） method in positive mode. The ion pairs for quantitative analysis are R⁃gentiandiol （m/z 210.04→192.06）， S⁃gentiandiol （m/z 210.04→192.06） and gentianone （m/z 192.02→162.08）. Results： The linear correlation coefficients of the method developed were greater than 0.999， the precision was less than 7.00%， the recovery was 99.57%⁃102.65 %， and the matrix effect was 90.94%⁃91.34 %. The peak tmax of R⁃gentiandiol and S⁃gentiandiol in rat plasma after oral administration of swertiamarin were （1.63±0.23 h and （1.58 ± 0.21） h， t1/2 was （6.23±0.52） h and （5.46±0.38） h， Cmax was （86.79±20.81） ng/mL and （60.72±18.95） ng/mL， and the AUC0⁃24 were （1 094.58±86.37）） （ng·h）/mL and （724.67±58.38） （ng·h）/mL， respectively. Conclusion： The method was highly sensitive with good accuracy and precision， and it was successfully applied for chiral resolution and pharmacokinetics study of R⁃gentiandiol and S⁃gentiandiol in plasma. The method developed and experimental results will provide scientific basis for the study of pharmacodynamics and pharmacodynamic material basis of swertiamarin， and lay a foundation for clinical application and resource development of TCM monomer.
Objective： A chiral resolution method for enantiomers of two chiral nitrogen⁃containing metabolites R⁃gentiandiol and S⁃gentiandiol of swertiamarin in plasma was developed， and the pharmacokinetics of the metabolites were studied. Methods： The metabolites of swertiamarin in vivo were detected by LC⁃MS/MS using Astec Cyclobond Ⅱ Cyclodextrin column （4.6 mm×100 mm， 5 μm）， gradient elution with acetonitrile⁃water as mobile phase， and monitored by multiple reaction monitoring （MRM） method in positive mode. The ion pairs for quantitative analysis are R⁃gentiandiol （m/z 210.04→192.06）， S⁃gentiandiol （m/z 210.04→192.06） and gentianone （m/z 192.02→162.08）. Results： The linear correlation coefficients of the method developed were greater than 0.999， the precision was less than 7.00%， the recovery was 99.57%⁃102.65 %， and the matrix effect was 90.94%⁃91.34 %. The peak tmax of R⁃gentiandiol and S⁃gentiandiol in rat plasma after oral administration of swertiamarin were （1.63±0.23 h and （1.58 ± 0.21） h， t1/2 was （6.23±0.52） h and （5.46±0.38） h， Cmax was （86.79±20.81） ng/mL and （60.72±18.95） ng/mL， and the AUC0⁃24 were （1 094.58±86.37）） （ng·h）/mL and （724.67±58.38） （ng·h）/mL， respectively. Conclusion： The method was highly sensitive with good accuracy and precision， and it was successfully applied for chiral resolution and pharmacokinetics study of R⁃gentiandiol and S⁃gentiandiol in plasma. The method developed and experimental results will provide scientific basis for the study of pharmacodynamics and pharmacodynamic material basis of swertiamarin， and lay a foundation for clinical application and resource development of TCM monomer.
WEI Wu?jun, WANG Chun?fang, JIANG Qi, XU Gui?dan, HUANG Jing?jing, LIN Cheng, HU Ren?tong, CHANG Zheng?yi
2023,29(6):8-14, DOI: 10.13210/j.cnki.jhmu.20221221.001
Abstract:
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
2023,29(6):51-61, DOI: 10.13210/j.cnki.jhmu.20210713.001
Abstract:
Objective： To evaluate the clinical efficacy and safety of cinobufagin injection in the treatment of liver cancer. Methods： PubMed database， Embase database and Cochrane Library database， CNKI， Wanfang database， VIP database and Sinomed database were used to search for the randomized controlled trials of cinobufagin injection combined with Western medicine in the treatment of primary liver cancer. The retrieval time was from the establishment to December 15， 2020. Two independent researchers conducted systematic screening， literature inclusion and quality assessment of the articles according to the inclusion criteria， respectively. Meta‑analysis of the data was performed using RevMan 5.4 software. Results： A total of 30 studies with a total of 2 355 patients were included. Compared with conventional western medicine treatment， the clinical effective rate of Hububutin injection combined with western medicine was significantly higher ［RR=1.16，95%CI=（1.11，1.22），P<0.000 01］. It could effectively reduce the tumor size ［RR=1.33，95%CI=（1.17，1.51），P<0.000 01］， prolong the survival time of patients ［RR=1.41，95%CI=（1.31，1.52），P<0.000 01］， improve the quality of life ［RR=1.37，95%CI=（1.19，1.57），P<0.000 01］， improve the liver function of patients ［RR=-14.52，95%CI=（-16.15，-12.88），P<0.000 01］， and reduce the occurrence of adverse reactions ［RR=0.94，95%CI=（0.85，1.42），P=0.25］ such as bone marrow suppression ［RR=0.44，95%CI=（0.31，0.62），P<0.000 01］. Conclusion： Cinobufagin injection combined with western medicine therapy can effectively improve the clinical symptoms of primary liver cancer， and the safety is good. However， the methodological quality of the included literature is low， which affects the objectivity of the outcome， and it still needs to be verified by multi‑sample， multi‑center， randomized double‑blind controlled trial.
Objective： To evaluate the clinical efficacy and safety of cinobufagin injection in the treatment of liver cancer. Methods： PubMed database， Embase database and Cochrane Library database， CNKI， Wanfang database， VIP database and Sinomed database were used to search for the randomized controlled trials of cinobufagin injection combined with Western medicine in the treatment of primary liver cancer. The retrieval time was from the establishment to December 15， 2020. Two independent researchers conducted systematic screening， literature inclusion and quality assessment of the articles according to the inclusion criteria， respectively. Meta‑analysis of the data was performed using RevMan 5.4 software. Results： A total of 30 studies with a total of 2 355 patients were included. Compared with conventional western medicine treatment， the clinical effective rate of Hububutin injection combined with western medicine was significantly higher ［RR=1.16，95%CI=（1.11，1.22），P<0.000 01］. It could effectively reduce the tumor size ［RR=1.33，95%CI=（1.17，1.51），P<0.000 01］， prolong the survival time of patients ［RR=1.41，95%CI=（1.31，1.52），P<0.000 01］， improve the quality of life ［RR=1.37，95%CI=（1.19，1.57），P<0.000 01］， improve the liver function of patients ［RR=-14.52，95%CI=（-16.15，-12.88），P<0.000 01］， and reduce the occurrence of adverse reactions ［RR=0.94，95%CI=（0.85，1.42），P=0.25］ such as bone marrow suppression ［RR=0.44，95%CI=（0.31，0.62），P<0.000 01］. Conclusion： Cinobufagin injection combined with western medicine therapy can effectively improve the clinical symptoms of primary liver cancer， and the safety is good. However， the methodological quality of the included literature is low， which affects the objectivity of the outcome， and it still needs to be verified by multi‑sample， multi‑center， randomized double‑blind controlled trial.
YAN Dong?ming, LIANG Jian?tang, LIU Xiao?qian, LI Meng?yongwei, DING Shun, MENG Qing?wen, ZHANG Si?yuan, TANG Cai?ying, LIU Qi?bing, YANG Kun
2023,29(6):28-36, DOI: 10.13210/j.cnki.jhmu.20221125.001
Abstract:
Objective： To investigate the prognostic value of ORMDL2 in human glioma and its relationship with immune invasion. Methods： The clinical survival data from TCGA – LGG&GBM， CGGA and GEO were used to evaluate the clinical prognostic value of ORMDL2. The cut off value of ORMDL2 was detected with pROC package to draw ROC curve to prove its value in differential diagnosis of glioma. The first 300 genes with the most significant positive correlation with ORMDL2 were selected to establish PPI network through STRING database and conduct GO and pathway analysis. The relationship between the expression of ORMDL2 mRNA and immune cell infiltration was investigated by using ssGSEA and TIMER2.0 databases. Results： The expression of ORMDL2 mRNA in glioma was significantly higher than that in adjacent normal tissues， and the difference was most significant in high‑grade glioma. The expression of ORMDL2 was increased in human glioma， which was related to the clinicopathological characteristics and poor prognosis of glioma patients. In addition， the increased expression of ORMDL2 was associated with a series of immune infiltrating cells， including macrophages. Conclusion： ORMDL2 plays an important role in glioma immune cell infiltration and is a biomarker of prognosis of glioma patients.
Objective： To investigate the prognostic value of ORMDL2 in human glioma and its relationship with immune invasion. Methods： The clinical survival data from TCGA – LGG&GBM， CGGA and GEO were used to evaluate the clinical prognostic value of ORMDL2. The cut off value of ORMDL2 was detected with pROC package to draw ROC curve to prove its value in differential diagnosis of glioma. The first 300 genes with the most significant positive correlation with ORMDL2 were selected to establish PPI network through STRING database and conduct GO and pathway analysis. The relationship between the expression of ORMDL2 mRNA and immune cell infiltration was investigated by using ssGSEA and TIMER2.0 databases. Results： The expression of ORMDL2 mRNA in glioma was significantly higher than that in adjacent normal tissues， and the difference was most significant in high‑grade glioma. The expression of ORMDL2 was increased in human glioma， which was related to the clinicopathological characteristics and poor prognosis of glioma patients. In addition， the increased expression of ORMDL2 was associated with a series of immune infiltrating cells， including macrophages. Conclusion： ORMDL2 plays an important role in glioma immune cell infiltration and is a biomarker of prognosis of glioma patients.
2021,27(11):872-875, DOI: 10.13210/j.cnki.jhmu.20200714.001
Abstract:
Drug resistance is a major problem when using molecular targeted drugs for tumors. Currently， functional gene screening is the most common strategy for screening drug resistance genes. In recent years， CRISPR‑Cas9 gene‑editing technology has been widely used in functional studies on tumor‑related genes because of its high accuracy， simplicity， and efficiency. In this paper， the principle of CRISPR‑Cas9 library screening technology and its application in functional gene screening are reviewed. At the same time， the application prospect of the CRISPR‑Cas9 technology is forecasted.
Drug resistance is a major problem when using molecular targeted drugs for tumors. Currently， functional gene screening is the most common strategy for screening drug resistance genes. In recent years， CRISPR‑Cas9 gene‑editing technology has been widely used in functional studies on tumor‑related genes because of its high accuracy， simplicity， and efficiency. In this paper， the principle of CRISPR‑Cas9 library screening technology and its application in functional gene screening are reviewed. At the same time， the application prospect of the CRISPR‑Cas9 technology is forecasted.
2023,29(6):1-7, DOI: 10.13210/j.cnki.jhmu.20230106.001
Abstract:
Objective：To explore the establishment of an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells. Methods： SH‑SY5Y cells were randomly divided into control （D‑galactose 0 mmol/L group）， D‑galactose （25 mmol/L， 50 mmol/L， 100 mmol/L， 200 mmol/L， 400 mmol/L） groups， and treated with corresponding concentrations of D‑galactose for 48 h. The changes of cell morphology， β‑galactosidase， the cell morphology， β‑galactosidase activity by microscopic observation， cell proliferation rate by EdU kit and cell survival rate by CCK‑8 assay were used to determine the decaying concentration of D‑galactose and to establish the senescence model. The senescent SH‑SY5Y cells were randomly divided into control group （oxygen glucose deprivation without treatment group）， oxygen glucose deprivation treatment （0.5 h， 1 h， 1.5 h， 2 h） group， followed by re‑glucose reoxygenation for 24 h， and CCK‑8 assay for the survival rate of senescent SH‑SY5Y cells. Results： There were no significant changes in cell morphology and β‑gal activity in the 25 mmol/L and 50 mmol/L groups compared with the control group （P>0.05）， cytosolic hypertrophy was seen in the cells of the 100 mmol/L group， chromatin fixation in the cells of the 200 mmol/L group， and massive vacuolization in the cells of the 400 mmol/L group； the positive rate of β‑galactosidase staining in the cells of the （100-400 mmol/L） group was significantly higher compared with the control group （P< 0.05）， with little difference between the 100 mmol/L and 200 mmol/L groups （P>0.05）； the cell proliferation ability of the （100-400 mmol/L） group was significantly decreased in a concentration‑dependent manner （P<0.05）； the cell survival rate was decreased in a concentration‑dependent manner （P<0.05）， with IC50 between 100 mmol/L and 200 mmol/L. The survival of senescent SH‑SY5Y cells showed a time‑dependent decrease in oxygen‑glucose deprivation （P<0.05）， with an IC50 close to 1 h. Conclusion： D‑gal concentration of 100 mmoL/L and 48 h of cell action could establish a survival rate of about 50% of senescent SH‑SY5Y cells， and oxygen glucose deprivation of senescent SH‑SY5Y cells for 1 h and reperfusion for 24 h could establish an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells with a survival rate close to 50%.
Objective：To explore the establishment of an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells. Methods： SH‑SY5Y cells were randomly divided into control （D‑galactose 0 mmol/L group）， D‑galactose （25 mmol/L， 50 mmol/L， 100 mmol/L， 200 mmol/L， 400 mmol/L） groups， and treated with corresponding concentrations of D‑galactose for 48 h. The changes of cell morphology， β‑galactosidase， the cell morphology， β‑galactosidase activity by microscopic observation， cell proliferation rate by EdU kit and cell survival rate by CCK‑8 assay were used to determine the decaying concentration of D‑galactose and to establish the senescence model. The senescent SH‑SY5Y cells were randomly divided into control group （oxygen glucose deprivation without treatment group）， oxygen glucose deprivation treatment （0.5 h， 1 h， 1.5 h， 2 h） group， followed by re‑glucose reoxygenation for 24 h， and CCK‑8 assay for the survival rate of senescent SH‑SY5Y cells. Results： There were no significant changes in cell morphology and β‑gal activity in the 25 mmol/L and 50 mmol/L groups compared with the control group （P>0.05）， cytosolic hypertrophy was seen in the cells of the 100 mmol/L group， chromatin fixation in the cells of the 200 mmol/L group， and massive vacuolization in the cells of the 400 mmol/L group； the positive rate of β‑galactosidase staining in the cells of the （100-400 mmol/L） group was significantly higher compared with the control group （P< 0.05）， with little difference between the 100 mmol/L and 200 mmol/L groups （P>0.05）； the cell proliferation ability of the （100-400 mmol/L） group was significantly decreased in a concentration‑dependent manner （P<0.05）； the cell survival rate was decreased in a concentration‑dependent manner （P<0.05）， with IC50 between 100 mmol/L and 200 mmol/L. The survival of senescent SH‑SY5Y cells showed a time‑dependent decrease in oxygen‑glucose deprivation （P<0.05）， with an IC50 close to 1 h. Conclusion： D‑gal concentration of 100 mmoL/L and 48 h of cell action could establish a survival rate of about 50% of senescent SH‑SY5Y cells， and oxygen glucose deprivation of senescent SH‑SY5Y cells for 1 h and reperfusion for 24 h could establish an oxygen glucose deprivation/reperfusion model of senescent SH‑SY5Y cells with a survival rate close to 50%.
2024,30(6):475-480, DOI: 10.13210/j.cnki.jhmu.20230804.003
Abstract:
Hepatocellular carcinoma （HCC） is one of the most common malignant tumors in the world. Its formation is a complex process， and the specific mechanism of its formation hasn't been cleared yet. Due to the fact that most HCC patients are diagnosed in the late stage， and they often lose good surgical opportunities. The emergence of targeted drugs has brought new hope to current HCC patients and can also serve as one of the measures for postoperative treatment， playing a huge role in treating HCC. Sorafenib is the first targeted drug used to treat HCC. It can induce apoptosis of liver tumor cells and inhibit proliferation and angiogenesis of liver tumor cells， so it can improve the survival rate of some patients. However， according to current research， 50% ⁃60% of HCC patients experience a decrease in sensitivity to the drug. It is mainly because Sorafenib will inhibit relevant signaling pathways in vivo after using， which leads to the occurrence of drug resistance， so further exploring the mechanism of Sorafenib resistance and reversing Sorafenib resistance have extremely important clinical value for improving the prognosis of liver cancer treatment. In recent years， many scholars have devoted themselves to studying the close relationship between Sorafenib mediated autophagy and drug resistance through Hippo/YAP and PI3K/Akt/mTOR signaling pathways. And exploring the molecular mechanisms of drug resistance has led to significant development in this field. Therefore， this article mainly discusses the relationship between Hippo/YAP and PI3K/Akt/mTOR signaling pathways and autophagy， as well as the mechanism of drug resistance mediated by them， so as to provide a reliable Scientific theory basis for drug resistance of Sorafenib in the treatment of liver cancer.
Hepatocellular carcinoma （HCC） is one of the most common malignant tumors in the world. Its formation is a complex process， and the specific mechanism of its formation hasn't been cleared yet. Due to the fact that most HCC patients are diagnosed in the late stage， and they often lose good surgical opportunities. The emergence of targeted drugs has brought new hope to current HCC patients and can also serve as one of the measures for postoperative treatment， playing a huge role in treating HCC. Sorafenib is the first targeted drug used to treat HCC. It can induce apoptosis of liver tumor cells and inhibit proliferation and angiogenesis of liver tumor cells， so it can improve the survival rate of some patients. However， according to current research， 50% ⁃60% of HCC patients experience a decrease in sensitivity to the drug. It is mainly because Sorafenib will inhibit relevant signaling pathways in vivo after using， which leads to the occurrence of drug resistance， so further exploring the mechanism of Sorafenib resistance and reversing Sorafenib resistance have extremely important clinical value for improving the prognosis of liver cancer treatment. In recent years， many scholars have devoted themselves to studying the close relationship between Sorafenib mediated autophagy and drug resistance through Hippo/YAP and PI3K/Akt/mTOR signaling pathways. And exploring the molecular mechanisms of drug resistance has led to significant development in this field. Therefore， this article mainly discusses the relationship between Hippo/YAP and PI3K/Akt/mTOR signaling pathways and autophagy， as well as the mechanism of drug resistance mediated by them， so as to provide a reliable Scientific theory basis for drug resistance of Sorafenib in the treatment of liver cancer.
2021,27(7):555-560, DOI: 10.13210/j.cnki.jhmu.20200930.003
Abstract:
Ulcerative colitis （UC） is a type of chronic inflammatory recurrent disease. The etiology and pathogenesis are still unclear by now. Among them， immune factors are usually considered to be the final link in the pathogenesis of UC. Due to the increasing incidence， long course of the disease， and difficult recovery， the relevant research is gradually deepened， and related research on intestinal flora， immunity， genetics， etc. has become a hot spot. A large amount of evidence indicates that regulatory T cells （Treg）， helper T cells 17 （Th17）， Th17/Treg immune axis and intestinal microbiota in UC patients play an important role in regulating the development of diseases. There is also a certain correlation between the bacterial flora and the Th17/Treg immune axis. Therefore， this article examines Th17/Treg cells， intestinal microbiota and the relationship between them by consulting a large number of relevant data at home and abroad in recent years. The formation of the immune axis and other issues are briefly summarized， with a view to providing more practical basis for clinical targeted therapy.
Ulcerative colitis （UC） is a type of chronic inflammatory recurrent disease. The etiology and pathogenesis are still unclear by now. Among them， immune factors are usually considered to be the final link in the pathogenesis of UC. Due to the increasing incidence， long course of the disease， and difficult recovery， the relevant research is gradually deepened， and related research on intestinal flora， immunity， genetics， etc. has become a hot spot. A large amount of evidence indicates that regulatory T cells （Treg）， helper T cells 17 （Th17）， Th17/Treg immune axis and intestinal microbiota in UC patients play an important role in regulating the development of diseases. There is also a certain correlation between the bacterial flora and the Th17/Treg immune axis. Therefore， this article examines Th17/Treg cells， intestinal microbiota and the relationship between them by consulting a large number of relevant data at home and abroad in recent years. The formation of the immune axis and other issues are briefly summarized， with a view to providing more practical basis for clinical targeted therapy.
CHEN Huan?xiong, HE Xian?bo, LI Guo?jun, TANG Song?jie, ZHONG Zhen?hao，, HUANG Tao, LIN You?cai, LIN Su?yu, MENG Zhi?bin
2023,29(6):43-50, DOI: 10.13210/j.cnki.jhmu.20230116.001
Abstract:
Objective： To study the position and the grade of screw perforation in the apical region of adolescent idiopathic scoliosis （AIS） surgery using a calibration technique for the intraoperative navigation error， and to analyze the related factors of navigation deviation and the clinical significance of the calibration technique. Methods： From 2017 to 2020， a total of 60 Lenke 1 AIS surgical cases were enrolled in this research. The 30 cases received surgery using the intraoperative navigation system （Navigation group） and another 30 cases were assisted with intraoperative navigation system with calibration technique （Calibration group） for the intraoperative navigation error. The basic information and radiological data of the both groups were all recorded. According to the Fu Chang⁃feng’s pedicle channel classification system， the pedicle on the apical region of the two groups was classified. And then the accuracy of screw placement of the two groups was evaluated according to the Rao’s classification. Results： A total of 600 screws were placed in the two groups. The 297 and 303 pedicle screws were implanted in the navigation group and the calibration group， respectively. In the apical region of the calibration group， the rates of the grade 0 screw placement in type A， B and C pedicle were 95.7%， 86.7% and 68.9% respectively. It was a statistically significant difference from the 73.9%， 66.9% and 30.0% in the navigation group respectively （P<0.05）. In the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 1.6%， 1.6% and 0%， respectively. The corresponding rates were 16.3%， 16.9%， 30.0% and 47.6% in the navigation group， respectively. Moreover， in the concave side of the apical region of the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 3.6%， 2.6% and 0%， respectively. Compared with the calibration group， the corresponding rates were higher in the navigation group （34.4%， 25.9%， 37.2% and 60.0%， respectively）. No serious complications such as spinal cord or neurovascular injury occurred for the two groups. Conclusion： Compared with the intraoperative navigation system， the calibration technique for the intraoperative navigation error could provide the higher accuracy of pedicle screw placement in the apical region of the major curve， the lower medial cortical perforation rate， the less screws misplacement rate on the concave side and the less complication rate of the severe Lenke 1 AIS patients.
Objective： To study the position and the grade of screw perforation in the apical region of adolescent idiopathic scoliosis （AIS） surgery using a calibration technique for the intraoperative navigation error， and to analyze the related factors of navigation deviation and the clinical significance of the calibration technique. Methods： From 2017 to 2020， a total of 60 Lenke 1 AIS surgical cases were enrolled in this research. The 30 cases received surgery using the intraoperative navigation system （Navigation group） and another 30 cases were assisted with intraoperative navigation system with calibration technique （Calibration group） for the intraoperative navigation error. The basic information and radiological data of the both groups were all recorded. According to the Fu Chang⁃feng’s pedicle channel classification system， the pedicle on the apical region of the two groups was classified. And then the accuracy of screw placement of the two groups was evaluated according to the Rao’s classification. Results： A total of 600 screws were placed in the two groups. The 297 and 303 pedicle screws were implanted in the navigation group and the calibration group， respectively. In the apical region of the calibration group， the rates of the grade 0 screw placement in type A， B and C pedicle were 95.7%， 86.7% and 68.9% respectively. It was a statistically significant difference from the 73.9%， 66.9% and 30.0% in the navigation group respectively （P<0.05）. In the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 1.6%， 1.6% and 0%， respectively. The corresponding rates were 16.3%， 16.9%， 30.0% and 47.6% in the navigation group， respectively. Moreover， in the concave side of the apical region of the calibration group， the rates of the medial cortical perforation in the type A， B， C and D pedicle were 0%， 3.6%， 2.6% and 0%， respectively. Compared with the calibration group， the corresponding rates were higher in the navigation group （34.4%， 25.9%， 37.2% and 60.0%， respectively）. No serious complications such as spinal cord or neurovascular injury occurred for the two groups. Conclusion： Compared with the intraoperative navigation system， the calibration technique for the intraoperative navigation error could provide the higher accuracy of pedicle screw placement in the apical region of the major curve， the lower medial cortical perforation rate， the less screws misplacement rate on the concave side and the less complication rate of the severe Lenke 1 AIS patients.
2023,29(6):15-21, DOI: 10.13210/j.cnki.jhmu.20211221.002
Abstract:
Objective： To investigate whether "Fuzheng Qingretonglin" decoction can reduce urinary tract damage caused by complex urinary tract infection caused by drug resistant Escherichia coli by regulating Nod‑like receptor pyrin domain3 inflammasome， and to explore the feasibility of this decoction combined with levofloxacin in the treatment of complex urinary tract infection caused by drug resistant bacteria. Methods： SD rats were divided into five groups： sham group， model group， levofloxacin group（Lev group）， levofloxacin+Fuzheng Qingre Tonglin decoction group（FZ+lev group）， and Fuzheng Qingre Tonglin decoction group（FZQRTL group）. After the experiment， urine was taken for bacterial culture to determine the urinary tract infection of rats in each group； HE staining was used to observe the pathological changes of kidney and bladder tissues in rats； The expression of NLRP3 in kidney and bladder tissues was detected by immunohistochemistry； The expression of IL‑1β and IL‑18 in serum of rats was detected by ELISA； The expressions of NLRP3，ASC and Caspase‑1 were detected by Western blotting. Results： The positive rate of urine bacteria culture in the sham group was 0%， the positive rate of urine bacteria culture in the model group was 100%； and the positive rate of urine bacteria culture in the FZ+lev group was 37.50%， which was statistically different from that in the model group（P<0.05）. A large number of inflammatory cells were observed in the kidney and bladder tissues of the model group by HE staining， while the number of inflammatory cells in the kidney and bladder tissues of the Lev group and FZQRTL group was significantly reduced compared with that of the model group. The FZ+lev group in the number and structure of inflammatory cells in kidney and bladder were similar to the sham group. The NLRP3 immunohistochemistry of kidney and bladder tissue in FZ+lev groups and FZQRTL groups was significantly different from that in model group（P<0.001）. The levels of IL‑1β and IL‑18 in serum of Lev group，FZQRTL group and FZ+lev group were significantly decreased by ELISA compared with model group（P<0.001）. The levels of IL‑1β and IL‑18 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. The protein expressions of NLRP3， ASC and Caspase‑1 in the Lev group， FZQRTL group and FZ+lev group were significantly lower than those in the model group（P<0.001）. The protein expressions of NLRP3， ASC and Caspase‑1 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. Conclusion： "Fuzheng Qingretonglin" decoction may have a protective effect on the kidney and bladder of rats with complex urinary tract infection caused by drug‑resistant Escherichia coli by inhibiting the activation of NLRP3 inflammatory bodies， and TCM combined with levofloxacin has a better therapeutic effect than TCM or levofloxacin alone.
Objective： To investigate whether "Fuzheng Qingretonglin" decoction can reduce urinary tract damage caused by complex urinary tract infection caused by drug resistant Escherichia coli by regulating Nod‑like receptor pyrin domain3 inflammasome， and to explore the feasibility of this decoction combined with levofloxacin in the treatment of complex urinary tract infection caused by drug resistant bacteria. Methods： SD rats were divided into five groups： sham group， model group， levofloxacin group（Lev group）， levofloxacin+Fuzheng Qingre Tonglin decoction group（FZ+lev group）， and Fuzheng Qingre Tonglin decoction group（FZQRTL group）. After the experiment， urine was taken for bacterial culture to determine the urinary tract infection of rats in each group； HE staining was used to observe the pathological changes of kidney and bladder tissues in rats； The expression of NLRP3 in kidney and bladder tissues was detected by immunohistochemistry； The expression of IL‑1β and IL‑18 in serum of rats was detected by ELISA； The expressions of NLRP3，ASC and Caspase‑1 were detected by Western blotting. Results： The positive rate of urine bacteria culture in the sham group was 0%， the positive rate of urine bacteria culture in the model group was 100%； and the positive rate of urine bacteria culture in the FZ+lev group was 37.50%， which was statistically different from that in the model group（P<0.05）. A large number of inflammatory cells were observed in the kidney and bladder tissues of the model group by HE staining， while the number of inflammatory cells in the kidney and bladder tissues of the Lev group and FZQRTL group was significantly reduced compared with that of the model group. The FZ+lev group in the number and structure of inflammatory cells in kidney and bladder were similar to the sham group. The NLRP3 immunohistochemistry of kidney and bladder tissue in FZ+lev groups and FZQRTL groups was significantly different from that in model group（P<0.001）. The levels of IL‑1β and IL‑18 in serum of Lev group，FZQRTL group and FZ+lev group were significantly decreased by ELISA compared with model group（P<0.001）. The levels of IL‑1β and IL‑18 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. The protein expressions of NLRP3， ASC and Caspase‑1 in the Lev group， FZQRTL group and FZ+lev group were significantly lower than those in the model group（P<0.001）. The protein expressions of NLRP3， ASC and Caspase‑1 in the FZ+lev groups were significantly lower than in the Lev group and FZQRTL group， and the differences were statistically significant（P<0.05）. Conclusion： "Fuzheng Qingretonglin" decoction may have a protective effect on the kidney and bladder of rats with complex urinary tract infection caused by drug‑resistant Escherichia coli by inhibiting the activation of NLRP3 inflammatory bodies， and TCM combined with levofloxacin has a better therapeutic effect than TCM or levofloxacin alone.
2021,27(1):71-74, DOI: 10．13210／j．cnki．jhmu．20200430．003
Abstract:
Endometriosis is not only a common disease in gynecology，but also a chronic and intractable disease in gy－ necology．In recent years，with the increase of cesarean section rate and the increase of artificial abortion and hysteroscopic op－ eration，the incidence of endometriosis has increased significantly，which impacts on women＇s health and quality of life．Treat－ ments of endometriosis by western medicine mainly include hormone therapy and surgical treatment，which have many limita－ tions and adverse reactions．In recent years，traditional Chinese medicine has shown more and more unique advantages，with di－ versification．We summarized literatures about the treatment of endometriosis with traditional Chinese medicine in recent years．
Endometriosis is not only a common disease in gynecology，but also a chronic and intractable disease in gy－ necology．In recent years，with the increase of cesarean section rate and the increase of artificial abortion and hysteroscopic op－ eration，the incidence of endometriosis has increased significantly，which impacts on women＇s health and quality of life．Treat－ ments of endometriosis by western medicine mainly include hormone therapy and surgical treatment，which have many limita－ tions and adverse reactions．In recent years，traditional Chinese medicine has shown more and more unique advantages，with di－ versification．We summarized literatures about the treatment of endometriosis with traditional Chinese medicine in recent years．
The mechanism and application of specialized phagocytic cell burial function in chronic wound repair
2024,30(13):1035-1040, DOI: 10.13210/j.cnki.jhmu.20240005.001
Abstract:
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
2021,27(21):1652-1658, DOI: 10.13210/j.cnki.jhmu.20210609.001
Abstract:
Objective： To further understand the pathogenesis of psoriasis based on bioinformatics， gene set enrichment analysis （GSEA） and immune infiltration analysis were carried out on the microarray data of psoriasis expression profile. Methods： GSE6710 chip data were obtained from gene expression database （GEO）， and gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis were performed using GSEA software. A total of 22 kinds of immune cell gene expression matrices and R packages were downloaded from CIBERSOFT official website， and the immune cell infiltration matrix was obtained by R software and related graphs were drawn. Results： The pathways related to cell proliferation and innate immunity were highly expressed in psoriatic lesions， and some cancer‑related pathways were highly expressed in psoriatic lesions. Immunized cell infiltration analysis showed that activated memory T cells， follicular helper T cells， M0 macrophages and activated dendritic cells were up‑regulated in the psoriatic skin lesion group， and inactive mast cells were down‑regulated in the psoriatic skin lesion group. Activated dendritic cells were positively correlated with follicular helper T cells， activated mast cells were positively correlated with M0 macrophages. Inactivated mast cells were negatively correlated with activated memory T cells， M1 macrophages were negatively correlated with regulatory T cells， M0 macrophages were negatively correlated with inactive mast cells.Conclusion： Cell proliferation and innate immunity are of great significance in the pathogenesis of psoriasis. Immune cell infiltration analysis is generally consistent with the current psoriasis pathogenesis model. Macrophages and mast cells also play a certain role in psoriasis.
Objective： To further understand the pathogenesis of psoriasis based on bioinformatics， gene set enrichment analysis （GSEA） and immune infiltration analysis were carried out on the microarray data of psoriasis expression profile. Methods： GSE6710 chip data were obtained from gene expression database （GEO）， and gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis were performed using GSEA software. A total of 22 kinds of immune cell gene expression matrices and R packages were downloaded from CIBERSOFT official website， and the immune cell infiltration matrix was obtained by R software and related graphs were drawn. Results： The pathways related to cell proliferation and innate immunity were highly expressed in psoriatic lesions， and some cancer‑related pathways were highly expressed in psoriatic lesions. Immunized cell infiltration analysis showed that activated memory T cells， follicular helper T cells， M0 macrophages and activated dendritic cells were up‑regulated in the psoriatic skin lesion group， and inactive mast cells were down‑regulated in the psoriatic skin lesion group. Activated dendritic cells were positively correlated with follicular helper T cells， activated mast cells were positively correlated with M0 macrophages. Inactivated mast cells were negatively correlated with activated memory T cells， M1 macrophages were negatively correlated with regulatory T cells， M0 macrophages were negatively correlated with inactive mast cells.Conclusion： Cell proliferation and innate immunity are of great significance in the pathogenesis of psoriasis. Immune cell infiltration analysis is generally consistent with the current psoriasis pathogenesis model. Macrophages and mast cells also play a certain role in psoriasis.
2023,29(6):73-78, DOI: 10.13210/j.cnki.jhmu.20210701.001
Abstract:
Coronary no‑reflow phenomenon belongs to a type of coronary microcirculation disturbance， and its main pathogenic factors are vascular endothelial cell injury， microembolism and inflammatory reaction， which are corresponding to the pathogenesis of choroid injury， blood stasis and heat toxin in traditional Chinese medicine， such as NO， ET‑1， chemokine， IL and other cytokines. The degree of improvement of patients' symptoms and laboratory examination data provide a basis for traditional Chinese medicine compound prescription， monomer and traditional Chinese medicine characteristic therapy for the treatment of no-reflow phenomena（NRP）. Combined with related factors， the author summarizes the research progress of traditional Chinese medicine treatment of NRP in recent years， in order to provide clinical reference.
Coronary no‑reflow phenomenon belongs to a type of coronary microcirculation disturbance， and its main pathogenic factors are vascular endothelial cell injury， microembolism and inflammatory reaction， which are corresponding to the pathogenesis of choroid injury， blood stasis and heat toxin in traditional Chinese medicine， such as NO， ET‑1， chemokine， IL and other cytokines. The degree of improvement of patients' symptoms and laboratory examination data provide a basis for traditional Chinese medicine compound prescription， monomer and traditional Chinese medicine characteristic therapy for the treatment of no-reflow phenomena（NRP）. Combined with related factors， the author summarizes the research progress of traditional Chinese medicine treatment of NRP in recent years， in order to provide clinical reference.
2021,27(7):481-487, DOI: 10.13210/j.cnki.jhmu.20200914.003
Abstract:
Objective： To investigate to the effect of hypoxia and hypoxia/reoxygenation on ROS， MAPKs and cell apoptosis in H9c2 cardiomyocytes. Methods： H9c2 cells were treated with cobalt chloride （CoCl2） at different concentrations （150， 300， 450， 600， 900， 1 200， 2 400 µmol/L） for 4-48 h to establish the hypoxia and hypoxia/reoxygenation-induced cardiomyocyte injury model. H9c2 cell viability was detected by MTT， and the intracellular ROS level was measured by 2'，7'-dichlorofluorescin diacetate and dihydroethidium. In addition， the expression level of mitogen-activated protein kinases （MAPKs） （including phosphorylated JNK， ERK and p38） and caspase-3 was determined by Western blotting. Results： At 300-12 00 µmol/L， CoCl2 inhibited the cell viability in H9c2 cells in a concentration and time-dependent manner （P<0.01）. Compared with the control group， the ROS levels under hypoxia condition were significantly increased （P<0.05） at 4 and 16 h. Moreover， the expression levels of p-JNK， p-p38 and caspase-3 were increased （P<0.05）. However， the expression of p-ERK remained unchanged. Furthermore， the expression levels of ROS， p-JNK， p-ERK1/2， p-p38 and caspase-3 in the hypoxia/reoxygenation group were significantly increased compared with the hypoxia group （P<0.01）. Conclusion： Reoxygenation further aggravates hypoxia-induced oxidative stress injury in cardiomyocyte by activating ROS/MAPKs signaling pathway， suggesting the role of myocardial ischemia/reperfusion injury in the pathogenesis of ischemic heart disease.
Objective： To investigate to the effect of hypoxia and hypoxia/reoxygenation on ROS， MAPKs and cell apoptosis in H9c2 cardiomyocytes. Methods： H9c2 cells were treated with cobalt chloride （CoCl2） at different concentrations （150， 300， 450， 600， 900， 1 200， 2 400 µmol/L） for 4-48 h to establish the hypoxia and hypoxia/reoxygenation-induced cardiomyocyte injury model. H9c2 cell viability was detected by MTT， and the intracellular ROS level was measured by 2'，7'-dichlorofluorescin diacetate and dihydroethidium. In addition， the expression level of mitogen-activated protein kinases （MAPKs） （including phosphorylated JNK， ERK and p38） and caspase-3 was determined by Western blotting. Results： At 300-12 00 µmol/L， CoCl2 inhibited the cell viability in H9c2 cells in a concentration and time-dependent manner （P<0.01）. Compared with the control group， the ROS levels under hypoxia condition were significantly increased （P<0.05） at 4 and 16 h. Moreover， the expression levels of p-JNK， p-p38 and caspase-3 were increased （P<0.05）. However， the expression of p-ERK remained unchanged. Furthermore， the expression levels of ROS， p-JNK， p-ERK1/2， p-p38 and caspase-3 in the hypoxia/reoxygenation group were significantly increased compared with the hypoxia group （P<0.01）. Conclusion： Reoxygenation further aggravates hypoxia-induced oxidative stress injury in cardiomyocyte by activating ROS/MAPKs signaling pathway， suggesting the role of myocardial ischemia/reperfusion injury in the pathogenesis of ischemic heart disease.
External Links
Publication ethics
Mobile website
Copyright of website: Editorial Office of Journal of Hainan Medical University
