Journal of Hainan Medical University
Volume ,2026 Issue 5
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- 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
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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
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BA Qi, YAO Jiaxin, MENG Yuanyuan, KONG Yichen, TIAN Hao, GONG Wei, WANG Yuli, YANG Yang, GAO Chunsheng, YANG Meiyan
2026(5):321-329, DOI: 10.13210/j.cnki.jhmu.20250228.001
Abstract:
Objective:To prepare the antibacterial peptide FR‑13 loaded with chitosan thermosensitive hydrogel （FR‑13/CS）， and to investigate its physicochemical properties， antibacterial activity， and wound healing effects in mice， for providing a new strategy in treating skin injuries caused by battle wounds. Methods:The FR‑13/CS hydrogel was prepared using a physical crosslinking method， and its physicochemical properties were characterized by a scanning electron microscopy， rheology， mechanical testing， and in vitro degradation testing. Additionally， the biocompatibility and antibacterial effects of the FR‑13/CS hydrogel were evaluated. By using a full‑thickness skin wound model in mice， its effect on promoting wound healing was investigated. Results:The FR‑13/CS hydrogel exhibited excellent thermosensitive properties， a uniform microstructure， suitable mechanical strength， and good biodegradability. The results of in vitro antibacterial tests demonstrated that FR‑13/CS exhibited significant antibacterial activity against Escherichia coli and Staphylococcus aureus. In vivo pharmacodynamic experiments showed that the FR‑13/CS hydrogel significantly promoted wound healing in mice. Safety assessments confirmed that FR‑13/CS had good biocompatibility. Conclusion:The FR‑13/CS hydrogel possesses antibacterial activity and promotes wound healing， demonstrating a promising potential for clinical applications.
Objective:To prepare the antibacterial peptide FR‑13 loaded with chitosan thermosensitive hydrogel （FR‑13/CS）， and to investigate its physicochemical properties， antibacterial activity， and wound healing effects in mice， for providing a new strategy in treating skin injuries caused by battle wounds. Methods:The FR‑13/CS hydrogel was prepared using a physical crosslinking method， and its physicochemical properties were characterized by a scanning electron microscopy， rheology， mechanical testing， and in vitro degradation testing. Additionally， the biocompatibility and antibacterial effects of the FR‑13/CS hydrogel were evaluated. By using a full‑thickness skin wound model in mice， its effect on promoting wound healing was investigated. Results:The FR‑13/CS hydrogel exhibited excellent thermosensitive properties， a uniform microstructure， suitable mechanical strength， and good biodegradability. The results of in vitro antibacterial tests demonstrated that FR‑13/CS exhibited significant antibacterial activity against Escherichia coli and Staphylococcus aureus. In vivo pharmacodynamic experiments showed that the FR‑13/CS hydrogel significantly promoted wound healing in mice. Safety assessments confirmed that FR‑13/CS had good biocompatibility. Conclusion:The FR‑13/CS hydrogel possesses antibacterial activity and promotes wound healing， demonstrating a promising potential for clinical applications.
2026(5):330-338, DOI: 10.13210/j.cnki.jhmu.20250425.001
Abstract:
Objective:To investigate the effect of histone H3 modification on oxidative stress damage in hepatocellular carcinoma cells Hep3B in a cadmium‑exposed microenvironment. Methods:Hep3B were divided into a control group and a 20 ng/mL cadmium chloride （CdCl2） stained group， and cultured for 28 days. Flow cytometry was used to detect oxidative stress （reactive oxygen species，ROS） and apoptosis in each group at the time points of 7， 14， 21， and 28 day of culture； immunofluorescence was used to determine the expression of histone H3 acetylation in each group at different time points； scratches and CCK‑8 were used to determine the activity and proliferative capacity of cells in each group at different time points； and an inhibitor of histone H3 acetylation was used to intervene on the stained group at the 7， 14， and 21 day for 48 hours. Results:Cadmium exposure led to morphological atrophy， increased tentacle and fragmentation of Hep3B cells； cell migration and healing were slowed down； With prolonged cadmium exposure， ROS and apoptosis levels in the stained group increased significantly compared to those in the control group at the 7， 14， and 21 day （P<0.05）； there were no significant differences between the ROS and apoptosis levels in the stained group at 28 day and those in the control group （P>0.05）； Compared to the control groups， the expression level of protein H3 acetylation in the stained group at the 7 and 14 day significantly increased with the prolongation of the intervention time （P<0.01）， and the expression of protein H3 acetylation in the stained group at the 21 and 28 day tended to be in a steady state （P<0.01）； and the levels of apoptosis and ROS at the 7， 14， and 21 day inhibitor groups were decreased compared to those in the stained group （P<0.01）. Conclusion:Low‑dose cadmium exposure can induce oxidative stress injury leading to apoptosis in Hep3B hepatocellular carcinoma cells at an early stage， and inhibit the anti‑oxidative stress ability of hepatocellular carcinoma cells affecting their cellular activity； in long‑term low‑dose cadmium exposure， Hep3B hepatocellular carcinoma cells can enhance tolerance and adapt to the hazardous environment to maintain homeostasis through self‑regulation； histone H3 acetylation is involved in oxidative stress injury and apoptosis of Hep3B hepatocellular carcinoma cells.
Objective:To investigate the effect of histone H3 modification on oxidative stress damage in hepatocellular carcinoma cells Hep3B in a cadmium‑exposed microenvironment. Methods:Hep3B were divided into a control group and a 20 ng/mL cadmium chloride （CdCl2） stained group， and cultured for 28 days. Flow cytometry was used to detect oxidative stress （reactive oxygen species，ROS） and apoptosis in each group at the time points of 7， 14， 21， and 28 day of culture； immunofluorescence was used to determine the expression of histone H3 acetylation in each group at different time points； scratches and CCK‑8 were used to determine the activity and proliferative capacity of cells in each group at different time points； and an inhibitor of histone H3 acetylation was used to intervene on the stained group at the 7， 14， and 21 day for 48 hours. Results:Cadmium exposure led to morphological atrophy， increased tentacle and fragmentation of Hep3B cells； cell migration and healing were slowed down； With prolonged cadmium exposure， ROS and apoptosis levels in the stained group increased significantly compared to those in the control group at the 7， 14， and 21 day （P<0.05）； there were no significant differences between the ROS and apoptosis levels in the stained group at 28 day and those in the control group （P>0.05）； Compared to the control groups， the expression level of protein H3 acetylation in the stained group at the 7 and 14 day significantly increased with the prolongation of the intervention time （P<0.01）， and the expression of protein H3 acetylation in the stained group at the 21 and 28 day tended to be in a steady state （P<0.01）； and the levels of apoptosis and ROS at the 7， 14， and 21 day inhibitor groups were decreased compared to those in the stained group （P<0.01）. Conclusion:Low‑dose cadmium exposure can induce oxidative stress injury leading to apoptosis in Hep3B hepatocellular carcinoma cells at an early stage， and inhibit the anti‑oxidative stress ability of hepatocellular carcinoma cells affecting their cellular activity； in long‑term low‑dose cadmium exposure， Hep3B hepatocellular carcinoma cells can enhance tolerance and adapt to the hazardous environment to maintain homeostasis through self‑regulation； histone H3 acetylation is involved in oxidative stress injury and apoptosis of Hep3B hepatocellular carcinoma cells.
2026(5):339-344, DOI: 10.13210/j.cnki.jhmu.20250331.004
Abstract:
Objective:Autosis， as a form of autophagy dependent cell death， plays a contradictory role in promoting survival and promoting death in myocardial ischemia‑reperfusion injury （MIRI）. The aim of this study was to investigate the effect of annexin A2 （ANXA2） on MIRI and its mechanism by means of autosis. Methods:Cell hypoxia/reoxygenation （H/R） injury model was used to simulate MIRI， shRNA （shANXA2） targeting intervention was constructed， cell activity was detected by CCK‑8， the ratio of autophagosome to autophagolysosome was observed by confocal microscopy， and autosis related protein expression was detected by Western blot. Results:The expression of ANXA2 was significantly increased in cardiomyocytes after H/R injury， the expression of transcription factor EB （TFEB） was increased after downregulating ANXA2 expression， the proportion of autophagosomes was decreased， the proportion of lysosomes was increased， and cell viability was restored. Western blot results showed that down‑regulation of ANXA2 decreased the levels of ANXA2， P62 and LC3II， and up‑regulated the expression of TFEB. Conclusions:ANXA2 inhibits the expression of TFEB and nuclear translocation， affects autophagy flux and the occurrence of autosis， and aggravates the H/R injury of cardiomyocytes. Down‑regulation of ANXA2 promotes autophagy flux and reduces the occurrence of autosis， thereby alleviating MIRI. This study provides experimental evidence for ANXA2 as a potential target for the treatment of MIRI.
Objective:Autosis， as a form of autophagy dependent cell death， plays a contradictory role in promoting survival and promoting death in myocardial ischemia‑reperfusion injury （MIRI）. The aim of this study was to investigate the effect of annexin A2 （ANXA2） on MIRI and its mechanism by means of autosis. Methods:Cell hypoxia/reoxygenation （H/R） injury model was used to simulate MIRI， shRNA （shANXA2） targeting intervention was constructed， cell activity was detected by CCK‑8， the ratio of autophagosome to autophagolysosome was observed by confocal microscopy， and autosis related protein expression was detected by Western blot. Results:The expression of ANXA2 was significantly increased in cardiomyocytes after H/R injury， the expression of transcription factor EB （TFEB） was increased after downregulating ANXA2 expression， the proportion of autophagosomes was decreased， the proportion of lysosomes was increased， and cell viability was restored. Western blot results showed that down‑regulation of ANXA2 decreased the levels of ANXA2， P62 and LC3II， and up‑regulated the expression of TFEB. Conclusions:ANXA2 inhibits the expression of TFEB and nuclear translocation， affects autophagy flux and the occurrence of autosis， and aggravates the H/R injury of cardiomyocytes. Down‑regulation of ANXA2 promotes autophagy flux and reduces the occurrence of autosis， thereby alleviating MIRI. This study provides experimental evidence for ANXA2 as a potential target for the treatment of MIRI.
2026(5):345-354, DOI: 10.13210/j.cnki.jhmu.20251226.002
Abstract:
Objective:To investigate the mechanism of "Zhishen Tiaosui" acupuncture improving oxidative stress injury in rats with ischemic stroke （IS） through the Keap1/Nrf2/HO‑1 signaling axis. Methods:A total of 90 SPF male SD rats aged 6‒8 weeks （180‒220 g） were selected and divided into the sham operation group， the model group， the conventional acupuncture group， the "Zhishen Tiaosui" acupuncture group， and the Western medicine group （edaravone dexborneol group）， the middle cerebral artery occlusion （MCAO） model by modified suture method were established， the neurological deficit score was evaluated by Zea‑Longa neurological deficit score method， the cerebral infarction area was detected by TTC， the pathological damages of brain tissue were observed by H&E staining， the pathological changes of brain tissue were detected by Nissl staining， and the ultrastructure of ischemic brain tissue neurons， including mitochondrial morphology， was observed by transmission electron microscopy. The contents of total superoxide dismutase （T‑SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH‑PX）， and reactive oxygen species （ROS） in serum were detected by ELISA. The protein expression levels of Keap1， Nrf2， and HO‑1 in brain tissue were detected by Western blot. Results:Compared to the model group， the neurological function of the rats in the "Zhishen Tiaosui" acupuncture group were significantly improved， and the infarct area was reduced. Neuronal damage was alleviated， the number of Nissl bodies was increased， and the ultrastructure was improved. The levels of T‑SOD and GSH‑PX in serum were increased （P<0.01）， the contents of MDA and ROS were decreased （P<0.01）， the expression level of Keap1 protein in brain tissue was decreased （P<0.01）， and the expression levels of Nrf2 and HO‑1 proteins were increased （P<0.01）. Conclusion:The "Zhishen Tiaosui" acupuncture may effectively reduce the oxidative stress injury of IS rats through the Keap1/Nrf2/HO‑1 signaling axis. The therapeutic effect is comparable to that of edaravone dexborneol and is significantly better than that of conventional acupuncture. It provides a non‑drug effective alternative for clinical practice.
Objective:To investigate the mechanism of "Zhishen Tiaosui" acupuncture improving oxidative stress injury in rats with ischemic stroke （IS） through the Keap1/Nrf2/HO‑1 signaling axis. Methods:A total of 90 SPF male SD rats aged 6‒8 weeks （180‒220 g） were selected and divided into the sham operation group， the model group， the conventional acupuncture group， the "Zhishen Tiaosui" acupuncture group， and the Western medicine group （edaravone dexborneol group）， the middle cerebral artery occlusion （MCAO） model by modified suture method were established， the neurological deficit score was evaluated by Zea‑Longa neurological deficit score method， the cerebral infarction area was detected by TTC， the pathological damages of brain tissue were observed by H&E staining， the pathological changes of brain tissue were detected by Nissl staining， and the ultrastructure of ischemic brain tissue neurons， including mitochondrial morphology， was observed by transmission electron microscopy. The contents of total superoxide dismutase （T‑SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH‑PX）， and reactive oxygen species （ROS） in serum were detected by ELISA. The protein expression levels of Keap1， Nrf2， and HO‑1 in brain tissue were detected by Western blot. Results:Compared to the model group， the neurological function of the rats in the "Zhishen Tiaosui" acupuncture group were significantly improved， and the infarct area was reduced. Neuronal damage was alleviated， the number of Nissl bodies was increased， and the ultrastructure was improved. The levels of T‑SOD and GSH‑PX in serum were increased （P<0.01）， the contents of MDA and ROS were decreased （P<0.01）， the expression level of Keap1 protein in brain tissue was decreased （P<0.01）， and the expression levels of Nrf2 and HO‑1 proteins were increased （P<0.01）. Conclusion:The "Zhishen Tiaosui" acupuncture may effectively reduce the oxidative stress injury of IS rats through the Keap1/Nrf2/HO‑1 signaling axis. The therapeutic effect is comparable to that of edaravone dexborneol and is significantly better than that of conventional acupuncture. It provides a non‑drug effective alternative for clinical practice.
2026(5):355-361, DOI: 10.13210/j.cnki.jhmu.20250410.001
Abstract:
Objective:To observe the effects of Gandouling （GDL） on hepatic and serum exosomal long non‑coding RNA H19 （LncRNA H19） as well as cholestasis in hepatic tissues of copper‑loaded rats with Wilson disease， and to explore the mechanism of action of GDL ameliorating hepatic fibrosis in Wilson disease. Methods:A total of 60 SD male rats were randomly divided into the normal group （Control）， the model group （Model）， the GDL low‑dose group （GDL‑L）， the GDL medium‑dose group （GDL‑M）， the GDL high‑dose group （GDL‑H）， and the penicillamine group （PCA）， with 10 rats in each group. A copper‑loaded Wilson disease liver fibrosis model was constructed by feeding copper（Ⅱ） sulfate pentahydrate（CuSO4·5H2O）， and the drug was administered simultaneously during the modeling process. Each treatment group of GDL and the PCA group were administered the corresponding doses of the drugs by gavage， while the Control group and the Model group were administered an equal volume of distilled water by gavage for 30 consecutive days. H&E and Masson staining were used to observe the pathological changes in the liver. ELISA was utilized to measure cholestasis indicators， including γ‑glutamyl transferase （GGT）， alkaline phosphatase （ALP）， total bilirubin （TBIL）， and total bile acids （TBA）， as well as liver function markers alanine aminotransferase （ALT） and aspartate aminotransferase （AST）. Atomic absorption spectrophotometer was used to determine the copper content of bile. RT‑qPCR was used to detect the gene expressions of LncRNA H19， cytokeratin 7 （CK7）， an indicator of bile duct response， and cytokeratin 19 （CK19）； Western blot was used to observe the protein expressions of CK7 and CK19. Results:Compared to the Control group， the histopathologic pattern of liver tissue in the Model group showed unclear cell nucleus boundaries with lysis and necrosis， and obvious collagen deposition around the central vein and bile ducts of the liver tissue； the levels of ALT， AST， GGT， ALP， TBIL， TBA， and biliary copper were elevated significantly（P<0.01）. LncRNA H19， CK7， and CK19 gene expression levels increased significantly （P<0.01）. CK7 and CK19 protein levels increased significantly （P<0.01）.The degree of hepatic tissue fibrosis was significantly improved after the intervention of GDL and PCA. ALT， AST， GGT， ALP， TBL， TBA， and biliary copper levels were decreased （except for ALT、TBIL and TBA in the GDL‑L group）（P<0.01）， LncRNA H19， CK7， and CK19 gene expression levels were decreased （P<0.01）， and CK7 and CK19 protein levels were decreased （except for CK7 in the GDL‑L group）（P<0.05）. Conclusion:GDL may promote biliary copper excretion and ameliorate hepatic fibrosis in copper‑loaded rats with Wilson disease by regulating the expression of LncRNA H19.
Objective:To observe the effects of Gandouling （GDL） on hepatic and serum exosomal long non‑coding RNA H19 （LncRNA H19） as well as cholestasis in hepatic tissues of copper‑loaded rats with Wilson disease， and to explore the mechanism of action of GDL ameliorating hepatic fibrosis in Wilson disease. Methods:A total of 60 SD male rats were randomly divided into the normal group （Control）， the model group （Model）， the GDL low‑dose group （GDL‑L）， the GDL medium‑dose group （GDL‑M）， the GDL high‑dose group （GDL‑H）， and the penicillamine group （PCA）， with 10 rats in each group. A copper‑loaded Wilson disease liver fibrosis model was constructed by feeding copper（Ⅱ） sulfate pentahydrate（CuSO4·5H2O）， and the drug was administered simultaneously during the modeling process. Each treatment group of GDL and the PCA group were administered the corresponding doses of the drugs by gavage， while the Control group and the Model group were administered an equal volume of distilled water by gavage for 30 consecutive days. H&E and Masson staining were used to observe the pathological changes in the liver. ELISA was utilized to measure cholestasis indicators， including γ‑glutamyl transferase （GGT）， alkaline phosphatase （ALP）， total bilirubin （TBIL）， and total bile acids （TBA）， as well as liver function markers alanine aminotransferase （ALT） and aspartate aminotransferase （AST）. Atomic absorption spectrophotometer was used to determine the copper content of bile. RT‑qPCR was used to detect the gene expressions of LncRNA H19， cytokeratin 7 （CK7）， an indicator of bile duct response， and cytokeratin 19 （CK19）； Western blot was used to observe the protein expressions of CK7 and CK19. Results:Compared to the Control group， the histopathologic pattern of liver tissue in the Model group showed unclear cell nucleus boundaries with lysis and necrosis， and obvious collagen deposition around the central vein and bile ducts of the liver tissue； the levels of ALT， AST， GGT， ALP， TBIL， TBA， and biliary copper were elevated significantly（P<0.01）. LncRNA H19， CK7， and CK19 gene expression levels increased significantly （P<0.01）. CK7 and CK19 protein levels increased significantly （P<0.01）.The degree of hepatic tissue fibrosis was significantly improved after the intervention of GDL and PCA. ALT， AST， GGT， ALP， TBL， TBA， and biliary copper levels were decreased （except for ALT、TBIL and TBA in the GDL‑L group）（P<0.01）， LncRNA H19， CK7， and CK19 gene expression levels were decreased （P<0.01）， and CK7 and CK19 protein levels were decreased （except for CK7 in the GDL‑L group）（P<0.05）. Conclusion:GDL may promote biliary copper excretion and ameliorate hepatic fibrosis in copper‑loaded rats with Wilson disease by regulating the expression of LncRNA H19.
2026(5):362-371, DOI: 10.13210/j.cnki.jhmu.20241213.002
Abstract:
Objective:To investigate the effects of isorhamnetin （ISO） on the growth and migration of laryngeal cancer cells and its relationship with PI3K/AKT1/β‑catenin signaling. Methods:Laryngeal cancer cell lines （HEP‑2， TU212） and human colon epithelial cells （NCM460） were used as the research objects， the effects of ISO on the growth and migration of laryngeal cancer cells were analyzed by MTT assay， colony formation assay， scratch assay， Transwell assay， trypan blue staining， Hoechst 33258 staining， mitochondrial membrane potential detection， and reactive oxygen species detection； Network pharmacology and molecular docking were used to predict the molecular targets of ISO on laryngeal cancer cells； Western blot was used to detect the expressions of p‑PI3K， p‑AKT1， β‑catenin， and cyclin D1 protein in laryngeal cancer cells. Results:Compared to the control group （ISO 0 μmol/L）， ISO （10， 20， 40 μmol/L） significantly inhibited the proliferation， colony formation， migration， and invasion of HEP‑2 and TU212 cells， and induced the increase of reactive oxygen species level， the decrease of mitochondrial membrane potential， and the increase of apoptosis rate. The results of network pharmacology and molecular docking suggested that ISO may have effects on AKT1 molecular targets； Western blot results showed that the protein expression levels of p‑PI3K， p‑AKT1， β‑catenin， and cyclin D1 were significantly lower than those in the control group after HEP‑2 and TU212 cells were treated with different concentrations of ISO （10、20、40μmol/L）（P<0.05）. Conclusions:ISO can inhibit the growth and migration of laryngeal cancer cells， and induce apoptosis by increasing the level of reactive oxygen species and reducing mitochondrial membrane potential， and its molecular mechanism may be related to the regulation of PI3K/AKT1/β‑catenin signaling pathway.
Objective:To investigate the effects of isorhamnetin （ISO） on the growth and migration of laryngeal cancer cells and its relationship with PI3K/AKT1/β‑catenin signaling. Methods:Laryngeal cancer cell lines （HEP‑2， TU212） and human colon epithelial cells （NCM460） were used as the research objects， the effects of ISO on the growth and migration of laryngeal cancer cells were analyzed by MTT assay， colony formation assay， scratch assay， Transwell assay， trypan blue staining， Hoechst 33258 staining， mitochondrial membrane potential detection， and reactive oxygen species detection； Network pharmacology and molecular docking were used to predict the molecular targets of ISO on laryngeal cancer cells； Western blot was used to detect the expressions of p‑PI3K， p‑AKT1， β‑catenin， and cyclin D1 protein in laryngeal cancer cells. Results:Compared to the control group （ISO 0 μmol/L）， ISO （10， 20， 40 μmol/L） significantly inhibited the proliferation， colony formation， migration， and invasion of HEP‑2 and TU212 cells， and induced the increase of reactive oxygen species level， the decrease of mitochondrial membrane potential， and the increase of apoptosis rate. The results of network pharmacology and molecular docking suggested that ISO may have effects on AKT1 molecular targets； Western blot results showed that the protein expression levels of p‑PI3K， p‑AKT1， β‑catenin， and cyclin D1 were significantly lower than those in the control group after HEP‑2 and TU212 cells were treated with different concentrations of ISO （10、20、40μmol/L）（P<0.05）. Conclusions:ISO can inhibit the growth and migration of laryngeal cancer cells， and induce apoptosis by increasing the level of reactive oxygen species and reducing mitochondrial membrane potential， and its molecular mechanism may be related to the regulation of PI3K/AKT1/β‑catenin signaling pathway.
2026(5):372-382, DOI: 10.13210/j.cnki.jhmu.20250424.001
Abstract:
Objective:To determine the role of Rauvolfia verticillata in treating ulcerative colitis and the underlying mechanism. Methods:The active components of Rauvolfia verticillata were screened using the HERB database and relevant literature， and its potential targets were identified. The ulcerative colitis‑related targets were obtained from the GeneCards database. Subsequently， a component‑target network was constructed， and the Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathways were analyzed to investigate the potential mechanism of Rauvolfia verticillata in treating ulcerative colitis. Additionally， mice with dextran sulfate sodium （DSS）‑induced ulcerative colitis were utilized to evaluate the therapeutic effects and mechanism of Rauvolfia verticillata treating ulcerative colitis. Results:A total of 26 potential targets of Rauvolfia verticillata in ulcerative colitis were identified. The component‑target network analysis suggested that pectin may serve as a key component in ulcerative colitis treatment. The functional enrichment analysis indicated a strong association between the therapeutic effects of Rauvolfia verticillata on ulcerative colitis and the Janus kinase （JAK）‑signal transducer and activator of transcription （STAT） signaling pathway. In vivo experimental results demonstrated the effectiveness of Rauvolfia verticillata pectin in ameliorating clinical symptoms （e.g. disease activity index， colonic length， and pathological changes） and the reduction of tumor necrosis factor‑α （TNF‑α）， interleukin‑1β （IL‑1β）， and interleukin‑6 （IL‑6） expressions in mice with DSS‑induced ulcerative colitis （P<0.05）. Moreover， Rauvolfia verticillata pectin could downregulate JAK2 and STAT3 expressions within the JAK‑STAT signaling pathway（P<0.05）. Conclusions:Rauvolfia verticillata， particularly its pectin， might exert a therapeutic effect on ulcerative colitis by modulating the JAK‑STAT signaling pathway， thereby providing an experimental foundation for the application of Rauvolfia verticillata in ulcerative colitis treatment.
Objective:To determine the role of Rauvolfia verticillata in treating ulcerative colitis and the underlying mechanism. Methods:The active components of Rauvolfia verticillata were screened using the HERB database and relevant literature， and its potential targets were identified. The ulcerative colitis‑related targets were obtained from the GeneCards database. Subsequently， a component‑target network was constructed， and the Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathways were analyzed to investigate the potential mechanism of Rauvolfia verticillata in treating ulcerative colitis. Additionally， mice with dextran sulfate sodium （DSS）‑induced ulcerative colitis were utilized to evaluate the therapeutic effects and mechanism of Rauvolfia verticillata treating ulcerative colitis. Results:A total of 26 potential targets of Rauvolfia verticillata in ulcerative colitis were identified. The component‑target network analysis suggested that pectin may serve as a key component in ulcerative colitis treatment. The functional enrichment analysis indicated a strong association between the therapeutic effects of Rauvolfia verticillata on ulcerative colitis and the Janus kinase （JAK）‑signal transducer and activator of transcription （STAT） signaling pathway. In vivo experimental results demonstrated the effectiveness of Rauvolfia verticillata pectin in ameliorating clinical symptoms （e.g. disease activity index， colonic length， and pathological changes） and the reduction of tumor necrosis factor‑α （TNF‑α）， interleukin‑1β （IL‑1β）， and interleukin‑6 （IL‑6） expressions in mice with DSS‑induced ulcerative colitis （P<0.05）. Moreover， Rauvolfia verticillata pectin could downregulate JAK2 and STAT3 expressions within the JAK‑STAT signaling pathway（P<0.05）. Conclusions:Rauvolfia verticillata， particularly its pectin， might exert a therapeutic effect on ulcerative colitis by modulating the JAK‑STAT signaling pathway， thereby providing an experimental foundation for the application of Rauvolfia verticillata in ulcerative colitis treatment.
2026(5):383-390, DOI: 10.13210/j.cnki.jhmu.20250425.002
Abstract:
Objective:To analyze the potential mechanism by which CpG ODN adjuvants enhance the preventive effect of periodontitis gene vaccines at the molecular level by transcriptome sequencing and to screen out key genes and signaling pathways for follow‑up research. Methods:A total of nine 4‒6 week‑old male Sprague‑Dawley rats were randomly divided into three groups. The rats were immunized by intranasal instillation， and euthanize at the 7th week. After total RNA was extracted from the spleen， RNA‑seq library construction and sequencing were performed. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were used to screen for differentially expressed genes （DEGs）. The screened DEGs were transferred to the STRING database to establish a protein‑protein interaction （PPI） network map， and the Cytoscape software was used to further draw the network map. RT‑qPCR was used to validate key genes. Results:Based on GO， KEGG， and PPI， five key genes were screened， including Oas2， Irf 7， Np4， Defa11 and Camp. These candidate genes may play a key role in the immune mechanism of periodontitis gene vaccines. The verification of key genes by RT‑qPCR showed that the results of the experiment were consistent with the transcriptome sequencing analysis. Conclusion:The results of the experiment are consistent with the transcriptome sequencing analysis of the preventive effect of periodontitis gene vaccines based on transcriptomic sequencing， and screens out five key genes involved in the synergistic effect of CpG ODN adjuvant with periodontitis gene vaccines， which provides a preliminary exploration of the immune mechanism of periodontitis genetic vaccines at the genetic level.
Objective:To analyze the potential mechanism by which CpG ODN adjuvants enhance the preventive effect of periodontitis gene vaccines at the molecular level by transcriptome sequencing and to screen out key genes and signaling pathways for follow‑up research. Methods:A total of nine 4‒6 week‑old male Sprague‑Dawley rats were randomly divided into three groups. The rats were immunized by intranasal instillation， and euthanize at the 7th week. After total RNA was extracted from the spleen， RNA‑seq library construction and sequencing were performed. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were used to screen for differentially expressed genes （DEGs）. The screened DEGs were transferred to the STRING database to establish a protein‑protein interaction （PPI） network map， and the Cytoscape software was used to further draw the network map. RT‑qPCR was used to validate key genes. Results:Based on GO， KEGG， and PPI， five key genes were screened， including Oas2， Irf 7， Np4， Defa11 and Camp. These candidate genes may play a key role in the immune mechanism of periodontitis gene vaccines. The verification of key genes by RT‑qPCR showed that the results of the experiment were consistent with the transcriptome sequencing analysis. Conclusion:The results of the experiment are consistent with the transcriptome sequencing analysis of the preventive effect of periodontitis gene vaccines based on transcriptomic sequencing， and screens out five key genes involved in the synergistic effect of CpG ODN adjuvant with periodontitis gene vaccines， which provides a preliminary exploration of the immune mechanism of periodontitis genetic vaccines at the genetic level.
WU Mingli, DAI Ting, WANG Jiayin, HAN Wen, FAN Wenyu, LI Yunpeng, FENG Huili, SHEN Xin, Lyu Zhuan, ZHANG Ming, GAO Jing, FENG Xiaodong
2026(5):391-400, DOI: 10.13210/j.cnki.jhmu.20250417.001
Abstract:
Objective:To investigate the correlation between the cognitive impairment of vascular cognitive impairment （VCI） patients and brain iron deposition and serum iron metabolism indexes， and to clarify the mechanism of cognitive impairment of VCI. Methods:A total of 42 patients with VCI and 21 age‑， gender‑， and education‑matched healthy controls were enrolled in this study. Montreal Cognitive Assessment （MoCA）， Mini‑mental State Examination （MMSE）， Modified Barthel Index （MBI）， and Clinical Dementia Rating （CDR） were used to assess cognitive function； magnetic resonance magnetic susceptibility‑weighted imaging （SWI） was used to check the signal intensity values of bilateral caudate nucleus， putamen， globus pallidus， thalamus， red nucleus， substantia nigra， and hippocampus in the brain； Enzyme‑linked immunosorbent assay was used to detect serum iron metabolism indicators such as serum iron， ferritin， transferrin， total iron‑binding capacity， and hemoglobin levels. The differences of SWI iron deposition and serum iron metabolism indexes between VCI patients and healthy controls were analyzed， and their correlations with cognitive function MoCA and MMSE scale scores were also analyzed. Results:There were no significant differences in age， gender， and baseline education between the two groups （P>0.05）. The MoCA， MMSE， MBI， and CDR scores of the VCI patients were significantly lower than those of the healthy controls （P<0.05）. There were significant differences in SWI signal intensity values in the left putamen， right substantia nigra， and left hippocampus between the VCI patients and the healthy controls （P<0.05）， and the SWI signal intensity value in the left hippocampus of the VCI patients was positively correlated with the total score of MoCA （r=0.311， P=0.045）. There were significant differences in serum iron， serum ferritin， serum transferrin， and total iron binding capacity between the VCI patients and the healthy controls （P<0.05）， and the serum ferritin level of VCI patients was negatively correlated with the total score of MoCA （r=-0.566， P<0.001）， suggesting that cognitive impairment in the VCI patients was associated with increased iron deposition in the left hippocampus and increased serum ferritin level. Conclusion:Iron homeostasis imbalance may be an important pathological mechanism of VCI， mainly manifested by increased iron deposition in the central nervous system and increased serum ferritin level.
Objective:To investigate the correlation between the cognitive impairment of vascular cognitive impairment （VCI） patients and brain iron deposition and serum iron metabolism indexes， and to clarify the mechanism of cognitive impairment of VCI. Methods:A total of 42 patients with VCI and 21 age‑， gender‑， and education‑matched healthy controls were enrolled in this study. Montreal Cognitive Assessment （MoCA）， Mini‑mental State Examination （MMSE）， Modified Barthel Index （MBI）， and Clinical Dementia Rating （CDR） were used to assess cognitive function； magnetic resonance magnetic susceptibility‑weighted imaging （SWI） was used to check the signal intensity values of bilateral caudate nucleus， putamen， globus pallidus， thalamus， red nucleus， substantia nigra， and hippocampus in the brain； Enzyme‑linked immunosorbent assay was used to detect serum iron metabolism indicators such as serum iron， ferritin， transferrin， total iron‑binding capacity， and hemoglobin levels. The differences of SWI iron deposition and serum iron metabolism indexes between VCI patients and healthy controls were analyzed， and their correlations with cognitive function MoCA and MMSE scale scores were also analyzed. Results:There were no significant differences in age， gender， and baseline education between the two groups （P>0.05）. The MoCA， MMSE， MBI， and CDR scores of the VCI patients were significantly lower than those of the healthy controls （P<0.05）. There were significant differences in SWI signal intensity values in the left putamen， right substantia nigra， and left hippocampus between the VCI patients and the healthy controls （P<0.05）， and the SWI signal intensity value in the left hippocampus of the VCI patients was positively correlated with the total score of MoCA （r=0.311， P=0.045）. There were significant differences in serum iron， serum ferritin， serum transferrin， and total iron binding capacity between the VCI patients and the healthy controls （P<0.05）， and the serum ferritin level of VCI patients was negatively correlated with the total score of MoCA （r=-0.566， P<0.001）， suggesting that cognitive impairment in the VCI patients was associated with increased iron deposition in the left hippocampus and increased serum ferritin level. Conclusion:Iron homeostasis imbalance may be an important pathological mechanism of VCI， mainly manifested by increased iron deposition in the central nervous system and increased serum ferritin level.
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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.
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.
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.
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．
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.
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.
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.
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%.
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.
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.
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.
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.
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