Journal of Hainan Medical University
Volume ,2024 Issue 19
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- Exploring the action mechanisms of Areca catechu L against diabetes mellitus with neurodegenerative diseases using network pharmacology and experimental verification
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2024(19):1441-1450, DOI: 10.13210/j.cnki.jhmu.20240524.002
Abstract:
Objective:To investigate how Xiaoxianxiong decoction can protect against intestinal damage caused by 5‑fluorouracil （5‑FU） in mice. Methods:One hundred male ICR breed mice with SPF‑grade were randomised into the normal control group, the model group and the low, medium and high dose （8.3, 16.6 and 33.2 g/kg） groups of Xiaoxianxiong decoction. Intestinal mucosal injury was induced in all groups, except the control group, by administering 5‑FU （30 mg/kg, ip, 7 d）. While modeling was ongoing, the mice in the Xiaoxianxiong decoction group were administered 10 mL·kg‑1·d‑1 via gavage, following the prescribed dosage. The control and model groups were administered equal volume of distilled water and treated continuously for 7 d. Histopathological alterations in the small intestine were assessed utilizing hematoxylin‑eosin staining （HE）, with the villus height to crypt depth ratio （VH：CD） subsequently determined. The number of goblet cells in the small intestinal mucosa was determined by Alcian blue staining （AB）. The concentrations of endotoxin （ET） and D‑lactic acid （D‑LA） in serum were measured using spectrophotometry, along with diamine oxidase （DAO） levels in the small intestine. The levels of interleukin‑6 （IL‑6） and tumor necrosis factor‑α （TNF‑α） in serum were detected using enzyme‑linked immunosorbent assay （ELISA）.The mRNA expression of IL‑6, signal transducer and activator of transcription 3 （STAT3）, and epidermal growth factor receptor （EGFR） was detected using reverse transcription quantitative polymerase chain reaction （RT‑qPCR）. The IL‑6, STAT3 and EGFR protein were expression in small intestinal tissues were detected by the Western blot method. Results:Compared to the control group, the model group of mice presented a significant reduction in body mass and an increase in scores for diarrhoea, faecal mass, faecal water content, and small intestinal propulsion rates.（P<0.01）. The VH：CD ratio, as well as the number of goblet cells in the small intestinal mucosa, exhibited a noteworthy decrease （P<0.01）. The levels of ET and D‑LA in the serum significantly augmented, while the level of DAO in the small intestine was significantly decreased （P<0.05）. Significant reductions were observed in the indices for the spleen and thymus （P<0.01）. A significant increase was observed in the serum levels of IL‑6 and TNFα（P<0.05）. IL‑6 and STAT3 mRNA expression were significantly up‑regulated, whilst EGFR mRNA expression was down‑regulated in small bowel tissues（P<0.01）. The expression of IL‑6 and STAT3 proteins was found to be significantly higher, while that of EGFR proteins was significantly lower, in small intestinal tissues （P<0.01）. Compared to the model group, Xiaoxianxiong decoction led to a significant improvement in the aforementioned indices （P<0.05）. Conclusion:Xiaoxianxiong decoction can safeguard the intestinal mucosa against damage caused by 5‑FU. The mechanism of action may involve the activation of EGFR signalling, down‑regulation of the IL‑6/STAT3 signalling pathway, reduction of 5‑FU‑induced inflammation of the intestinal mucosa, and improvement of immune function.
Objective:To investigate how Xiaoxianxiong decoction can protect against intestinal damage caused by 5‑fluorouracil （5‑FU） in mice. Methods:One hundred male ICR breed mice with SPF‑grade were randomised into the normal control group, the model group and the low, medium and high dose （8.3, 16.6 and 33.2 g/kg） groups of Xiaoxianxiong decoction. Intestinal mucosal injury was induced in all groups, except the control group, by administering 5‑FU （30 mg/kg, ip, 7 d）. While modeling was ongoing, the mice in the Xiaoxianxiong decoction group were administered 10 mL·kg‑1·d‑1 via gavage, following the prescribed dosage. The control and model groups were administered equal volume of distilled water and treated continuously for 7 d. Histopathological alterations in the small intestine were assessed utilizing hematoxylin‑eosin staining （HE）, with the villus height to crypt depth ratio （VH：CD） subsequently determined. The number of goblet cells in the small intestinal mucosa was determined by Alcian blue staining （AB）. The concentrations of endotoxin （ET） and D‑lactic acid （D‑LA） in serum were measured using spectrophotometry, along with diamine oxidase （DAO） levels in the small intestine. The levels of interleukin‑6 （IL‑6） and tumor necrosis factor‑α （TNF‑α） in serum were detected using enzyme‑linked immunosorbent assay （ELISA）.The mRNA expression of IL‑6, signal transducer and activator of transcription 3 （STAT3）, and epidermal growth factor receptor （EGFR） was detected using reverse transcription quantitative polymerase chain reaction （RT‑qPCR）. The IL‑6, STAT3 and EGFR protein were expression in small intestinal tissues were detected by the Western blot method. Results:Compared to the control group, the model group of mice presented a significant reduction in body mass and an increase in scores for diarrhoea, faecal mass, faecal water content, and small intestinal propulsion rates.（P<0.01）. The VH：CD ratio, as well as the number of goblet cells in the small intestinal mucosa, exhibited a noteworthy decrease （P<0.01）. The levels of ET and D‑LA in the serum significantly augmented, while the level of DAO in the small intestine was significantly decreased （P<0.05）. Significant reductions were observed in the indices for the spleen and thymus （P<0.01）. A significant increase was observed in the serum levels of IL‑6 and TNFα（P<0.05）. IL‑6 and STAT3 mRNA expression were significantly up‑regulated, whilst EGFR mRNA expression was down‑regulated in small bowel tissues（P<0.01）. The expression of IL‑6 and STAT3 proteins was found to be significantly higher, while that of EGFR proteins was significantly lower, in small intestinal tissues （P<0.01）. Compared to the model group, Xiaoxianxiong decoction led to a significant improvement in the aforementioned indices （P<0.05）. Conclusion:Xiaoxianxiong decoction can safeguard the intestinal mucosa against damage caused by 5‑FU. The mechanism of action may involve the activation of EGFR signalling, down‑regulation of the IL‑6/STAT3 signalling pathway, reduction of 5‑FU‑induced inflammation of the intestinal mucosa, and improvement of immune function.
2024(19):1451-1458, DOI: 10.13210/j.cnki.jhmu.20240527.002
Abstract:
Objective:To observe the impact of acupoint catgut embedding at Xinshu combined with trimetazidine on energy metabolism after myocardial infarction （MI） in rats.: Methods:The MI rat model was constructed by the typical ligation of the left anterior descending branch of the coronary artery, and the successfully-modeled rats were randomly divided into the model group, the catgut embedding group, the western medicine group, and the combined group, another single thoracotomy without ligation was used as the sham operation group. The intervention was started on the second day after operation, and the observation was carried out at two different time points of 7 d and 28 d after operation. The pathological morphology of myocardial tissue was observed by hematoxylin-eosin （H&E） staining, the content of adenosine triphosphate （ATP） in myocardial tissue and the concentration of free fatty acid （FFA） in serum were determined by biochemical detection, and the expression of AMPK and GLUT4 in myocardial tissue was detected by western blot. Results:In model group at 7 d and 28 d after model construction, the myocardial cells were swollen and disorganized, and obvious punctate inflammatory cell infiltration were seen compared with the sham peration group. Cardiomyocyte cross-sectional area and serum FFA concentration were increased, and myocardial ATP content and expression of AMPK and GLUT4 were decreased （all P<0.05）. At 7 d and 28 d after operation, compared with the model group, the morphology and arrangement of myocardial cells and the degree of inflammatory cell infiltration in the three treatment groups were improved to varying degrees, the cross-sectional area of myocardial cells and the concentration of serum FFA were decreased to varying degrees, and the content of myocardial ATP and the expression of AMPK and GLUT4 protein were increased to varying degrees （all P<0.05）, and the curative effect of the combined group was more obvious than that of the catgut embedding group and the western medicine group （P<0.05）. Compared with the treatment groups at 7 d after operation, the cross-sectional area of myocardial cells, myocardial ATP content and myocardial AMPK and GLUT4 protein expression in each treatment group increased at 28 d after operation （all P<0.05）, and the improvement effect of the combined group was the most obvious （P<0.05）. Conclusion:Acupoint catgut embedding at Xinshu combined with trimetazidine can further exert the protective effect on the myocardium after MI, and the combined application of the two has a synergistic effect. The mechanism may be to increase the expression of AMPK and GLUT4 protein in myocardial tissue, reduce serum FFA concentration and increase myocardial ATP content to improve myocardial energy metabolism disorder after MI, thereby improving cardiomyocyte hypertrophy and promoting myocardial injury repair.
Objective:To observe the impact of acupoint catgut embedding at Xinshu combined with trimetazidine on energy metabolism after myocardial infarction （MI） in rats.: Methods:The MI rat model was constructed by the typical ligation of the left anterior descending branch of the coronary artery, and the successfully-modeled rats were randomly divided into the model group, the catgut embedding group, the western medicine group, and the combined group, another single thoracotomy without ligation was used as the sham operation group. The intervention was started on the second day after operation, and the observation was carried out at two different time points of 7 d and 28 d after operation. The pathological morphology of myocardial tissue was observed by hematoxylin-eosin （H&E） staining, the content of adenosine triphosphate （ATP） in myocardial tissue and the concentration of free fatty acid （FFA） in serum were determined by biochemical detection, and the expression of AMPK and GLUT4 in myocardial tissue was detected by western blot. Results:In model group at 7 d and 28 d after model construction, the myocardial cells were swollen and disorganized, and obvious punctate inflammatory cell infiltration were seen compared with the sham peration group. Cardiomyocyte cross-sectional area and serum FFA concentration were increased, and myocardial ATP content and expression of AMPK and GLUT4 were decreased （all P<0.05）. At 7 d and 28 d after operation, compared with the model group, the morphology and arrangement of myocardial cells and the degree of inflammatory cell infiltration in the three treatment groups were improved to varying degrees, the cross-sectional area of myocardial cells and the concentration of serum FFA were decreased to varying degrees, and the content of myocardial ATP and the expression of AMPK and GLUT4 protein were increased to varying degrees （all P<0.05）, and the curative effect of the combined group was more obvious than that of the catgut embedding group and the western medicine group （P<0.05）. Compared with the treatment groups at 7 d after operation, the cross-sectional area of myocardial cells, myocardial ATP content and myocardial AMPK and GLUT4 protein expression in each treatment group increased at 28 d after operation （all P<0.05）, and the improvement effect of the combined group was the most obvious （P<0.05）. Conclusion:Acupoint catgut embedding at Xinshu combined with trimetazidine can further exert the protective effect on the myocardium after MI, and the combined application of the two has a synergistic effect. The mechanism may be to increase the expression of AMPK and GLUT4 protein in myocardial tissue, reduce serum FFA concentration and increase myocardial ATP content to improve myocardial energy metabolism disorder after MI, thereby improving cardiomyocyte hypertrophy and promoting myocardial injury repair.
LIU Yuxin, WANG Yameng, CHENG Simin, ZHU Ziyue, JIN Meiling, ZHAO Deping, XU Hongdan, LEI Xia, ZHANG Ning
2024(19):1459-1467, DOI: 10.13210/j.cnki.jhmu.20240511.001
Abstract:
Objective:To explore the mechanism of Rhizoma Anemarrhenae‑Cortex Phellodendri （AP） in ameliorating cognitive dysfunction in D‑galactose （D‑gal） model mice by observing the expression level of autophagy‑related proteins in the hippocampus. Methods:Seventy‑five mice were randomly divided into blank group, model group, piracetam group, AP group and autophagy inducer everolimus （RAD001） group. Except for the blank group, all the other groups were injected with 0.125 g∙kg‑1∙d‑1 D‑gal intraperitoneally to replicate the cognitive impairment model. The cognitive dysfunction of mice was tested by water maze experiment. The neuron status and Nissl bodies of hippocampus in each group were observed by HE staining and Nissl corpuscle number. The expression of LC3 and P62 positive cells in hippocampus was detected by immunohistochemistry. The relative expression levels of autophagy‑related proteins such as ULK1, LC3, Beclin‑1 and P62 were detected by Western Blot. The genes such as ULK1, Beclin‑1 and P62 were detected by real‑time fluorescence quantitative PCR. Results:Compared with the blank group, the learning memory ability of mice in the model group was significantly reduced, and neurons and Nissl bodies in hippocampal CA1 area were seriously lost and arranged in disorder. The expression of ULK1, LC3, Beclin‑1 protein and gene in hippocampus increased （P<0.01, P<0.05）, while the expression of P62 protein and gene decreased （P<0.01）. Compared with the model group, the learning memory ability of mice in the piracetam and AP groups was significantly improved, and the loss of neurons and Nissl bodies decreased. The expression of ULK1, LC3, Beclin‑1 protein and gene in hippocampus decreased （P<0.01）, while the expression of P62 protein and gene increased （P<0.01）. RAD001 group showed that AP could partially reverse the autophagy of cells after administration. Conclusion:AP can improve the cognitive dysfunction of D‑gal model mice, and its mechanism may be achieved by inhibiting autophagy of hippocampal cells.
Objective:To explore the mechanism of Rhizoma Anemarrhenae‑Cortex Phellodendri （AP） in ameliorating cognitive dysfunction in D‑galactose （D‑gal） model mice by observing the expression level of autophagy‑related proteins in the hippocampus. Methods:Seventy‑five mice were randomly divided into blank group, model group, piracetam group, AP group and autophagy inducer everolimus （RAD001） group. Except for the blank group, all the other groups were injected with 0.125 g∙kg‑1∙d‑1 D‑gal intraperitoneally to replicate the cognitive impairment model. The cognitive dysfunction of mice was tested by water maze experiment. The neuron status and Nissl bodies of hippocampus in each group were observed by HE staining and Nissl corpuscle number. The expression of LC3 and P62 positive cells in hippocampus was detected by immunohistochemistry. The relative expression levels of autophagy‑related proteins such as ULK1, LC3, Beclin‑1 and P62 were detected by Western Blot. The genes such as ULK1, Beclin‑1 and P62 were detected by real‑time fluorescence quantitative PCR. Results:Compared with the blank group, the learning memory ability of mice in the model group was significantly reduced, and neurons and Nissl bodies in hippocampal CA1 area were seriously lost and arranged in disorder. The expression of ULK1, LC3, Beclin‑1 protein and gene in hippocampus increased （P<0.01, P<0.05）, while the expression of P62 protein and gene decreased （P<0.01）. Compared with the model group, the learning memory ability of mice in the piracetam and AP groups was significantly improved, and the loss of neurons and Nissl bodies decreased. The expression of ULK1, LC3, Beclin‑1 protein and gene in hippocampus decreased （P<0.01）, while the expression of P62 protein and gene increased （P<0.01）. RAD001 group showed that AP could partially reverse the autophagy of cells after administration. Conclusion:AP can improve the cognitive dysfunction of D‑gal model mice, and its mechanism may be achieved by inhibiting autophagy of hippocampal cells.
2024(19):1468-1477, DOI: 10.13210/j.cnki.jhmu.20240530.002
Abstract:
Objective:To investigate the expression of NKD1 in colon cancer tissues and its correlation with clinicopathologic features in patients with colon cancer, and study the involvement of NKD1 in the migration of colon cancer cells and elucidate its precise mechanism in regulating the epithelial-mesenchymal transition （EMT）-related protein ZEB1. The findings of this study may contribute to the identification of novel therapeutic targets for metastatic colorectal cancer. Methods:Bioinformatics was used to analyze the expression of NKD1 in colon cancer cells and its correlation with clinical pathological characteristic factor. Through the collection of 98 pairs of colon cancer patient samples and relevant clinical information from Changzhou Wujin People’s Hospital, and after the verification of the bioinformatics results, the survival curve was drawn. Wound healing assay and Transwell assay were performed to prove that NKD1 promotes colon cancer cell migration. qPCR and Western lot experiments were used to confirm that NKD1 regulates ZEB1 at the protein level. Western blot and immunoprecipitation experiments were conducted to further study the specific mechanism of NKD1 regulation of ZEB1. Results:NKD1 was highly expressed in colon cancer tissues, and its expression level was correlated with clinical characteristics such as differentiation, tumor staging, and whether there was distant metastasis or not. The high expression of NKD1 was associated with poor prognosis in colon cancer patients. The overexpression of NKD1 promoted the migration of colon cancer cells, while the knockdown of NKD1 led to the opposite result. NKD1 regulated EB1 at the protein level and could maintain the protein stability of ZEB1. The high expression of NKD1 inhibited the autophagy degradation of ZEB1 by regulating the binding of ZEB1 to autophagy related protein LC3. Conclusion:NKD1 is associated with poor prognosis in patients with colon cancer, and can inhibit autophagy degradation of ZEB1 by regulating the binding of ZEB1 to autophagy associated protein LC3, thus promoting the migration of colon cancer cells.
Objective:To investigate the expression of NKD1 in colon cancer tissues and its correlation with clinicopathologic features in patients with colon cancer, and study the involvement of NKD1 in the migration of colon cancer cells and elucidate its precise mechanism in regulating the epithelial-mesenchymal transition （EMT）-related protein ZEB1. The findings of this study may contribute to the identification of novel therapeutic targets for metastatic colorectal cancer. Methods:Bioinformatics was used to analyze the expression of NKD1 in colon cancer cells and its correlation with clinical pathological characteristic factor. Through the collection of 98 pairs of colon cancer patient samples and relevant clinical information from Changzhou Wujin People’s Hospital, and after the verification of the bioinformatics results, the survival curve was drawn. Wound healing assay and Transwell assay were performed to prove that NKD1 promotes colon cancer cell migration. qPCR and Western lot experiments were used to confirm that NKD1 regulates ZEB1 at the protein level. Western blot and immunoprecipitation experiments were conducted to further study the specific mechanism of NKD1 regulation of ZEB1. Results:NKD1 was highly expressed in colon cancer tissues, and its expression level was correlated with clinical characteristics such as differentiation, tumor staging, and whether there was distant metastasis or not. The high expression of NKD1 was associated with poor prognosis in colon cancer patients. The overexpression of NKD1 promoted the migration of colon cancer cells, while the knockdown of NKD1 led to the opposite result. NKD1 regulated EB1 at the protein level and could maintain the protein stability of ZEB1. The high expression of NKD1 inhibited the autophagy degradation of ZEB1 by regulating the binding of ZEB1 to autophagy related protein LC3. Conclusion:NKD1 is associated with poor prognosis in patients with colon cancer, and can inhibit autophagy degradation of ZEB1 by regulating the binding of ZEB1 to autophagy associated protein LC3, thus promoting the migration of colon cancer cells.
2024(19):1478-1485, DOI: 10.13210/j.cnki.jhmu.20240527.003
Abstract:
Objective:To observe the effect of Bushen Qiangdu formula on CX3CL1/NF‑κB signaling pathway mediated polarization of M1 macrophages and elucidate its molecular mechanism in treating ankylosing spondylitis. Methods:Lipopolysaccharide （LPS）‑induced THP‑1 cells were used to construct a cell model, and Bushen Qiangdu medicated serum and CX3CL1 inhibitor AZD8797 were given for intervention. The levels of inflammatory factors （TNF‑α, IL‑6, IL‑1β and IL‑17） were detected by enzyme‑linked immunosorbent assay. CD86 expression was detected by flow cytometry. Expression of iNOS, osteoblast differentiation marker proteins （TRAP, calcitonin and p‑NFATC1β） and the CX3CL1/NF‑κB pathway was assessed by Western blot. The expression of iNOS mRNA was quantified by real‑time quantitative polymerase chain reaction （qRT‑PCR）. Results:Compared with the control group, the content of TNF‑α, IL‑6, IL‑1β, IL‑17 in macrophages and the proportion of CD86+ macrophages in the model group were significantly increased, and iNOS, CX3CL1, p‑P65, p‑IkKα/β, p‑IkBα, TRAP, calcitonin and p‑NFATC1β protein and iNOS mRNA expression were significantly upregulated, all of which were statistically significant （P<0.01）. Bushen Qiangdu-medicated serum significantly decreased the content of TNF‑α, IL‑6, IL‑1β, IL‑17 and the proportion of CD86+ macrophages, and down‑regulated the expression of iNOS, CX3CL1, p‑P65, p‑IKKα/β, p‑IkBα, TRAP, Calcitonin and p‑NFATC1β proteins and iNOS mRNA expression, which showed statistically significant differences compared with the model group （P<0.05）. Conclusion:Bushen Qiangdu formula inhibits M1 polarization of macrophages by inhibiting CX3CL1/NF‑κB signaling pathway, then playing a role of inhibiting inflammation and osteoclast differentiation in the treatment of ankylosing spondylitis.
Objective:To observe the effect of Bushen Qiangdu formula on CX3CL1/NF‑κB signaling pathway mediated polarization of M1 macrophages and elucidate its molecular mechanism in treating ankylosing spondylitis. Methods:Lipopolysaccharide （LPS）‑induced THP‑1 cells were used to construct a cell model, and Bushen Qiangdu medicated serum and CX3CL1 inhibitor AZD8797 were given for intervention. The levels of inflammatory factors （TNF‑α, IL‑6, IL‑1β and IL‑17） were detected by enzyme‑linked immunosorbent assay. CD86 expression was detected by flow cytometry. Expression of iNOS, osteoblast differentiation marker proteins （TRAP, calcitonin and p‑NFATC1β） and the CX3CL1/NF‑κB pathway was assessed by Western blot. The expression of iNOS mRNA was quantified by real‑time quantitative polymerase chain reaction （qRT‑PCR）. Results:Compared with the control group, the content of TNF‑α, IL‑6, IL‑1β, IL‑17 in macrophages and the proportion of CD86+ macrophages in the model group were significantly increased, and iNOS, CX3CL1, p‑P65, p‑IkKα/β, p‑IkBα, TRAP, calcitonin and p‑NFATC1β protein and iNOS mRNA expression were significantly upregulated, all of which were statistically significant （P<0.01）. Bushen Qiangdu-medicated serum significantly decreased the content of TNF‑α, IL‑6, IL‑1β, IL‑17 and the proportion of CD86+ macrophages, and down‑regulated the expression of iNOS, CX3CL1, p‑P65, p‑IKKα/β, p‑IkBα, TRAP, Calcitonin and p‑NFATC1β proteins and iNOS mRNA expression, which showed statistically significant differences compared with the model group （P<0.05）. Conclusion:Bushen Qiangdu formula inhibits M1 polarization of macrophages by inhibiting CX3CL1/NF‑κB signaling pathway, then playing a role of inhibiting inflammation and osteoclast differentiation in the treatment of ankylosing spondylitis.
2024(19):1486-1496, DOI: 10.13210/j.cnki.jhmu.20240518.002
Abstract:
Objective:To explore of the mechanism of Curculiginis Rhizoma, a traditional Chinese medicine, sensitizing lung cancer cells to cisplatin chemotherapy. Methods:Network pharmacology and molecular docking techniques were used to screen the main apoptotic proteins of Curculiginis Rhizoma in non‑small cell lung cancer； CCK‑8 assay was performed to measure cell proliferation rate； Western blot was used to detect the expression levels of cleaved Caspase3 and cleaved Caspase9 proteins in lung cancer cells （A549） after treatment with Curculiginis Rhizoma, cisplatin alone, and in combination； flow cytometry was used to detect the total apoptosis rate of cells； cell scratch and invasion experiments were conducted to assess cell migration and invasion capabilities. Results:At a concentration of 100‑1 500 μg/mL, the water extract of Curculiginis Rhizoma showed no significant inhibitory effect on the proliferation of A549 cells. However, the combined treatment showed a significantly enhanced inhibitory effect on A549 cells compared to cisplatin alone. Compared to the control group, the Curculiginis Rhizoma group and the combined treatment group demonstrated significantly increased expression levels of Caspase3 and Caspase9 proteins, total apoptosis rate, as well as cell migration and invasion inhibition rate. The cisplatin group showed significantly increased expression levels of Caspase3 and Caspase9 proteins, as well as the total apoptosis rate, compared to the control group. Additionally, compared to the cisplatin alone group, the Curculiginis Rhizoma group and the combined Curculiginis Rhizoma and cisplatin group demonstrated significantly increased expression of Caspase3 and Caspase9 proteins, total apoptosis rate, and cell migration and invasion inhibition rate. Conclusions:Curculiginis Rhizoma, cisplatin, and the combination of Curculiginis Rhizoma with cisplatin can induce apoptosis in A549 cells. The combination with Curculiginis Rhizoma enhances the induction of apoptosis by cisplatin in A549 cells, and its mechanism is related to the apoptosis‑associated proteins Caspase3 and Caspase9. Additionally, the combined treatment of Curculiginis Rhizoma followed by cisplatin shows a more pronounced inhibitory effect on the proliferation, migration, and invasion capabilities of A549 cells.
Objective:To explore of the mechanism of Curculiginis Rhizoma, a traditional Chinese medicine, sensitizing lung cancer cells to cisplatin chemotherapy. Methods:Network pharmacology and molecular docking techniques were used to screen the main apoptotic proteins of Curculiginis Rhizoma in non‑small cell lung cancer； CCK‑8 assay was performed to measure cell proliferation rate； Western blot was used to detect the expression levels of cleaved Caspase3 and cleaved Caspase9 proteins in lung cancer cells （A549） after treatment with Curculiginis Rhizoma, cisplatin alone, and in combination； flow cytometry was used to detect the total apoptosis rate of cells； cell scratch and invasion experiments were conducted to assess cell migration and invasion capabilities. Results:At a concentration of 100‑1 500 μg/mL, the water extract of Curculiginis Rhizoma showed no significant inhibitory effect on the proliferation of A549 cells. However, the combined treatment showed a significantly enhanced inhibitory effect on A549 cells compared to cisplatin alone. Compared to the control group, the Curculiginis Rhizoma group and the combined treatment group demonstrated significantly increased expression levels of Caspase3 and Caspase9 proteins, total apoptosis rate, as well as cell migration and invasion inhibition rate. The cisplatin group showed significantly increased expression levels of Caspase3 and Caspase9 proteins, as well as the total apoptosis rate, compared to the control group. Additionally, compared to the cisplatin alone group, the Curculiginis Rhizoma group and the combined Curculiginis Rhizoma and cisplatin group demonstrated significantly increased expression of Caspase3 and Caspase9 proteins, total apoptosis rate, and cell migration and invasion inhibition rate. Conclusions:Curculiginis Rhizoma, cisplatin, and the combination of Curculiginis Rhizoma with cisplatin can induce apoptosis in A549 cells. The combination with Curculiginis Rhizoma enhances the induction of apoptosis by cisplatin in A549 cells, and its mechanism is related to the apoptosis‑associated proteins Caspase3 and Caspase9. Additionally, the combined treatment of Curculiginis Rhizoma followed by cisplatin shows a more pronounced inhibitory effect on the proliferation, migration, and invasion capabilities of A549 cells.
2024(19):1497-1506, DOI: 10.13210/j.cnki.jhmu.20240202.002
Abstract:
Objective:Bayesian meta‑analysis was used to evaluate the effect of non‑drug intervention on alleviating the migration stress level of family members of patients transferred out of ICU. Methods:Databases including CNKI, Web of Science （SCIE）, Cochrane Library and Embase were searched by computer system to collect randomized controlled trials （RCTS） of different non‑drug interventions on alleviating migration stress of family members of ICU patients transferred from the database inception until June 2023. A mesh meta‑analysis was performed using Stata 15 software. Results:A total of 15 RCTS were included, and a total of 1 186 patients were studied, involving five non‑drug interventions. The results showed that in terms of English FRSS score, the effect of intervention measures to reduce the level of caregiver migration stress was ranked as behavior change round model >ICU contact nurse > Migration manual > Comprehensive nursing > cognitive behavioral intervention. In the Chinese version of FRSS score, the effect of intervention measures to reduce the level of caregiver migration stress was ranked as migration manual > cognitive behavioral intervention > Structured health education > comprehensive nursing. In terms of FCTI score, the effect of interventions to reduce the level of caregiver migration stress was ranked as behavior change round mode >ICU contact nurse > Migration manual > Comprehensive nursing. In terms of STAI score, the effect of interventions to reduce the level of caregiver migration stress was ranked as ICU contact nurse > Migration manual > Structured health education > Comprehensive nursing. Conclusion:Compared with comprehensive nursing alone, non‑drug intervention combined with comprehensive nursing has a better effect on alleviating the migration stress level of caregivers.
Objective:Bayesian meta‑analysis was used to evaluate the effect of non‑drug intervention on alleviating the migration stress level of family members of patients transferred out of ICU. Methods:Databases including CNKI, Web of Science （SCIE）, Cochrane Library and Embase were searched by computer system to collect randomized controlled trials （RCTS） of different non‑drug interventions on alleviating migration stress of family members of ICU patients transferred from the database inception until June 2023. A mesh meta‑analysis was performed using Stata 15 software. Results:A total of 15 RCTS were included, and a total of 1 186 patients were studied, involving five non‑drug interventions. The results showed that in terms of English FRSS score, the effect of intervention measures to reduce the level of caregiver migration stress was ranked as behavior change round model >ICU contact nurse > Migration manual > Comprehensive nursing > cognitive behavioral intervention. In the Chinese version of FRSS score, the effect of intervention measures to reduce the level of caregiver migration stress was ranked as migration manual > cognitive behavioral intervention > Structured health education > comprehensive nursing. In terms of FCTI score, the effect of interventions to reduce the level of caregiver migration stress was ranked as behavior change round mode >ICU contact nurse > Migration manual > Comprehensive nursing. In terms of STAI score, the effect of interventions to reduce the level of caregiver migration stress was ranked as ICU contact nurse > Migration manual > Structured health education > Comprehensive nursing. Conclusion:Compared with comprehensive nursing alone, non‑drug intervention combined with comprehensive nursing has a better effect on alleviating the migration stress level of caregivers.
2024(19):1507-1513, DOI: 10.13210/j.cnki.jhmu.20240508.001
Abstract:
Ferroptosis is a newly discovered cell death pattern characterized by pathway of reduction-oxidation in recent years. It is different from the classical pathways such as apoptosis, necrosis and autophagy in its mechanism and regulation of metabolism. With the in⁃depth study of tumor microenvironment and iron metabolism abnormalities in non⁃small cell lung cancer （NSCLC）, ferroptosis has attracted extensive attention in the academic community. This paper focuses on the regulatory mechanism of ferroptosis in the development of NSCLC, the effects of ferroptosis on the biological characteristics of NSCLC cells, and the role of ferroptosis in the immune microenvironment, aiming to further explore the possibility of ferroptosis as a clinical therapeutic target and provide new ideas for the development of therapeutic strategies for NSCLC.
Ferroptosis is a newly discovered cell death pattern characterized by pathway of reduction-oxidation in recent years. It is different from the classical pathways such as apoptosis, necrosis and autophagy in its mechanism and regulation of metabolism. With the in⁃depth study of tumor microenvironment and iron metabolism abnormalities in non⁃small cell lung cancer （NSCLC）, ferroptosis has attracted extensive attention in the academic community. This paper focuses on the regulatory mechanism of ferroptosis in the development of NSCLC, the effects of ferroptosis on the biological characteristics of NSCLC cells, and the role of ferroptosis in the immune microenvironment, aiming to further explore the possibility of ferroptosis as a clinical therapeutic target and provide new ideas for the development of therapeutic strategies for NSCLC.
2024(19):1514-1520, DOI: 10.13210/j.cnki.jhmu.20240530.001
Abstract:
The sweet taste receptor （STR） is a critical member of type 1 taste receptors that senses sweetness and is activated by different types of saccharides and artificial sweeteners. Although it was originally discovered in oral taste buds, recent findings have demonstrated their expression in extraoral tissues such as the myocardium, kidneys, pancreas, gastrointestinal tract, respiratory tract, and brain. They facilitate diverse biological functions, including the modulation of feeding activities, energy homeostasis, endocrine metabolism, endothelial permeability, immune defense, and cognitive function. In this review, the advancement in understanding the signaling pathways of STR and their biological roles in extraoral tissues was elucidated, aiming to provide a reference for future research.
The sweet taste receptor （STR） is a critical member of type 1 taste receptors that senses sweetness and is activated by different types of saccharides and artificial sweeteners. Although it was originally discovered in oral taste buds, recent findings have demonstrated their expression in extraoral tissues such as the myocardium, kidneys, pancreas, gastrointestinal tract, respiratory tract, and brain. They facilitate diverse biological functions, including the modulation of feeding activities, energy homeostasis, endocrine metabolism, endothelial permeability, immune defense, and cognitive function. In this review, the advancement in understanding the signaling pathways of STR and their biological roles in extraoral tissues was elucidated, aiming to provide a reference for future research.
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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.
2024(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(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(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．
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.
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(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(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.
2023(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%.
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(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.
WEI Wu?jun, WANG Chun?fang, JIANG Qi, XU Gui?dan, HUANG Jing?jing, LIN Cheng, HU Ren?tong, CHANG Zheng?yi
2023(6):8-14, DOI: 10.13210/j.cnki.jhmu.20221221.001
Abstract:
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
Objective： To investigate the effect of mir⁃3168 on the malignant transformation and cisplatin resistance of AGS and AGS/DDP gastric cancer cells， and to verify its target gene. Methods： The expression of mir⁃3168 in AGS and AGS/DDP gastric cancer cells was detected by qPCR， and mir⁃3168 mimic， inhibitor and negative control were synthesized. They were transfected into AGS and AGS/DDP gastric cancer cells， respectively. The expression of mir⁃3168 and TP53 mRNA was detected by qPCR. Cell viability was detected by CCK8 under gradient cisplatin treatment and non treatment， apoptosis was detected by flow cytometry， cell invasion was detected by Transwell， and TP53 protein expression was detected by western blot， The database predicted the binding sites of mir⁃3168 and TP53. According to the binding sites， the double luciferase experiment was used to verify the binding of mir⁃3168 and TP53. Results： Compared with cisplatin sensitive gastric cancer cell AGS， mir⁃3168 was significantly overexpressed in cisplatin resistant gastric cancer cell AGS/DDP； mir⁃3168 mimic promotes cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and inhibits apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 inhibitor inhibits cisplatin resistance， proliferation and invasion of AGS and AGS/DDP gastric cancer cells， and promotes apoptosis of AGS and AGS/DDP gastric cancer cells； mir⁃3168 mimic inhibits the expression of TP53 mRNA and protein， and mir⁃3168 inhibitor promotes the expression of TP53 mRNA and protein； Targetscan database predicted that there was a binding point between mir⁃3168 and TP53， and the double luciferase experiment suggested that mir⁃3168 was bound to TP53 through the predicted binding site. Conclusion： mir⁃3168 may promote the malignant transformation of AGS and AGS/DDP gastric cancer cells and cisplatin resistance by targeting TP53.
2023(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(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.
The mechanism and application of specialized phagocytic cell burial function in chronic wound repair
2024(13):1035-1040, DOI: 10.13210/j.cnki.jhmu.20240005.001
Abstract:
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
Chronic wounds， as a long‑term wasting disease， are a long‑term clinical problem that is difficult to solve. Dysfunction of efferocytosis prevents apoptotic cells from being cleared from the wound in time， resulting in secondary cell necrosis and release of pro‑inflammatory cytokines， making it difficult for the wound to transition from the inflammatory phase to the proliferative phase. Macrophages and dendritic cells， as professional phagocytes， are the main bearers of efferocytosis. This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis‑related receptors， macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM‑1， NK‑4， MIR‑21， CD36， etc.， to accelerate the healing of chronic wounds. In addition， the efferocytosis function of dendritic cells may be limited by SLC7A11. Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing. This study is of great significance to further elucidating the healing process of chronic refractory wound and the development of new treatmentss.
2021,27(21):1652-1658, DOI: 10.13210/j.cnki.jhmu.20210609.001
Abstract:
Objective： To further understand the pathogenesis of psoriasis based on bioinformatics， gene set enrichment analysis （GSEA） and immune infiltration analysis were carried out on the microarray data of psoriasis expression profile. Methods： GSE6710 chip data were obtained from gene expression database （GEO）， and gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis were performed using GSEA software. A total of 22 kinds of immune cell gene expression matrices and R packages were downloaded from CIBERSOFT official website， and the immune cell infiltration matrix was obtained by R software and related graphs were drawn. Results： The pathways related to cell proliferation and innate immunity were highly expressed in psoriatic lesions， and some cancer‑related pathways were highly expressed in psoriatic lesions. Immunized cell infiltration analysis showed that activated memory T cells， follicular helper T cells， M0 macrophages and activated dendritic cells were up‑regulated in the psoriatic skin lesion group， and inactive mast cells were down‑regulated in the psoriatic skin lesion group. Activated dendritic cells were positively correlated with follicular helper T cells， activated mast cells were positively correlated with M0 macrophages. Inactivated mast cells were negatively correlated with activated memory T cells， M1 macrophages were negatively correlated with regulatory T cells， M0 macrophages were negatively correlated with inactive mast cells.Conclusion： Cell proliferation and innate immunity are of great significance in the pathogenesis of psoriasis. Immune cell infiltration analysis is generally consistent with the current psoriasis pathogenesis model. Macrophages and mast cells also play a certain role in psoriasis.
Objective： To further understand the pathogenesis of psoriasis based on bioinformatics， gene set enrichment analysis （GSEA） and immune infiltration analysis were carried out on the microarray data of psoriasis expression profile. Methods： GSE6710 chip data were obtained from gene expression database （GEO）， and gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis were performed using GSEA software. A total of 22 kinds of immune cell gene expression matrices and R packages were downloaded from CIBERSOFT official website， and the immune cell infiltration matrix was obtained by R software and related graphs were drawn. Results： The pathways related to cell proliferation and innate immunity were highly expressed in psoriatic lesions， and some cancer‑related pathways were highly expressed in psoriatic lesions. Immunized cell infiltration analysis showed that activated memory T cells， follicular helper T cells， M0 macrophages and activated dendritic cells were up‑regulated in the psoriatic skin lesion group， and inactive mast cells were down‑regulated in the psoriatic skin lesion group. Activated dendritic cells were positively correlated with follicular helper T cells， activated mast cells were positively correlated with M0 macrophages. Inactivated mast cells were negatively correlated with activated memory T cells， M1 macrophages were negatively correlated with regulatory T cells， M0 macrophages were negatively correlated with inactive mast cells.Conclusion： Cell proliferation and innate immunity are of great significance in the pathogenesis of psoriasis. Immune cell infiltration analysis is generally consistent with the current psoriasis pathogenesis model. Macrophages and mast cells also play a certain role in psoriasis.
2023(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.
2022,28(3):235-240, DOI: 10.13210/j.cnki.jhmu.20201109.003
Abstract:
The pathogenesis of diabetic foot disease is complex and its clinical manifestations are diverse. Western medicine mainly focuses on hypoglycemic， improving circulation， controlling infection， interventional and surgical treatment， and the clinical effect is not good. Chinese medicine has obvious advantages in the treatment of diabetic foot， including syndrome differentiation， staging treatment， prescription plus or minus treatment， Chinese patent medicine， external foot bath， fumigation and washing， massage， acupuncture and moxibustion， ointment powder application and comprehensive treatment of traditional Chinese and western medicine. This paper discusses the treatment of diabetic foot with traditional Chinese medicine.
The pathogenesis of diabetic foot disease is complex and its clinical manifestations are diverse. Western medicine mainly focuses on hypoglycemic， improving circulation， controlling infection， interventional and surgical treatment， and the clinical effect is not good. Chinese medicine has obvious advantages in the treatment of diabetic foot， including syndrome differentiation， staging treatment， prescription plus or minus treatment， Chinese patent medicine， external foot bath， fumigation and washing， massage， acupuncture and moxibustion， ointment powder application and comprehensive treatment of traditional Chinese and western medicine. This paper discusses the treatment of diabetic foot with traditional Chinese medicine.
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