Objective: To investigate the effects of fucoidan inducing impairment of human osteosarcoma cell 143B, as well its mechanisms. Methods: After 143B cells were treated with different concentrations of FUC (0, 0.5, 1, 10, 100, 400, 800 μg/ml) for 48 h, the cell viability and dehydrogenase (LDH) level were detected by MTT assay and chemical colorimetry with six multiple wells for each concentration. Based on MTT results, we determined the value of IC50 was 244.5 μg/ml. The follow-up experiments were divided into control group (without FUC), FUC (10 μg/ml)-treated group, FUC (100 μg/ml)-treated group, FUC (400 μg/ml)-treated group and positive group (resveratrol, 40 μmol/L). There were four multiple wells for each concentration, and each experiment was repeated at least three times. Flow cytometry was performed to detect cell apoptosis and intracellular reactive oxygen species (ROS) level; acridine orange (AO) staining and lyso-tracker red staining were used to observe the autophagolysosome formation; chemical colorimetric analysis was performed to determine malondialdehyde (MDA) content and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); Western blot was used to detect protein expressions of nuclear factor E2-associated factor 2 (Nrf2), heme oxygenase 1 (HO-1) and autophagy-associated proteins including microtubule-associated light chain protein 3 (LC-3), Atg7, Beclin-1 and p62. Results: Compared with control group, the cell viability was decreased significantly in FUC (100～400 μg/ml)-treated groups (P＜0.01); LDH levels in the supernatant (P＜0.05 or P＜0.01), the percentage of cell apoptosis (P＜0.01), intracellular ROS level and MDA content (P＜0.01) were increased remarkably; protein expressions of Atg7 and Beclin-1 were upregulated (P＜0.05 or P＜0.01); the conversion from LC-3I to LC-3II was significant (P＜0.01) together with elevation of autophagolysosome formation (P＜0.05 or P＜0.01); while the activities of SOD and GSH-Px and protein expressions of Nrf2, HO-1 and p62 were decreased remarkably (P＜0.05 or P＜0.01). Conclusion: FUC (100～400 μg/ml) treatment induces oxidative damage and autophagic death in osteosarcoma 143B cells.
{"title":"[Effects of fucoidan inducing impairment of human osteosarcoma cell 143B and its mechanism].","authors":"Qi-Qi Wang, Qiao Lin, Wei-Yan Shan, Tao Zhang, Yu-Rong Li, Yun Zhang","doi":"10.12047/j.cjap.6331.2022.135","DOIUrl":"https://doi.org/10.12047/j.cjap.6331.2022.135","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects of fucoidan inducing impairment of human osteosarcoma cell 143B, as well its mechanisms. <b>Methods:</b> After 143B cells were treated with different concentrations of FUC (0, 0.5, 1, 10, 100, 400, 800 μg/ml) for 48 h, the cell viability and dehydrogenase (LDH) level were detected by MTT assay and chemical colorimetry with six multiple wells for each concentration. Based on MTT results, we determined the value of IC<sub>50</sub> was 244.5 μg/ml. The follow-up experiments were divided into control group (without FUC), FUC (10 μg/ml)-treated group, FUC (100 μg/ml)-treated group, FUC (400 μg/ml)-treated group and positive group (resveratrol, 40 μmol/L). There were four multiple wells for each concentration, and each experiment was repeated at least three times. Flow cytometry was performed to detect cell apoptosis and intracellular reactive oxygen species (ROS) level; acridine orange (AO) staining and lyso-tracker red staining were used to observe the autophagolysosome formation; chemical colorimetric analysis was performed to determine malondialdehyde (MDA) content and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); Western blot was used to detect protein expressions of nuclear factor E2-associated factor 2 (Nrf2), heme oxygenase 1 (HO-1) and autophagy-associated proteins including microtubule-associated light chain protein 3 (LC-3), Atg7, Beclin-1 and p62. <b>Results:</b> Compared with control group, the cell viability was decreased significantly in FUC (100～400 μg/ml)-treated groups (<i>P</i>＜0.01); LDH levels in the supernatant (<i>P</i>＜0.05 or <i>P</i>＜0.01), the percentage of cell apoptosis (<i>P</i>＜0.01), intracellular ROS level and MDA content (<i>P</i>＜0.01) were increased remarkably; protein expressions of Atg7 and Beclin-1 were upregulated (<i>P</i>＜0.05 or <i>P</i>＜0.01); the conversion from LC-3I to LC-3II was significant (<i>P</i>＜0.01) together with elevation of autophagolysosome formation (<i>P</i>＜0.05 or <i>P</i>＜0.01); while the activities of SOD and GSH-Px and protein expressions of Nrf2, HO-1 and p62 were decreased remarkably (<i>P</i>＜0.05 or <i>P</i>＜0.01). <b>Conclusion:</b> FUC (100～400 μg/ml) treatment induces oxidative damage and autophagic death in osteosarcoma 143B cells.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"739-744"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9618060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.12047/j.cjap.6327.2022.146
Yi Zhang, Chao Wu, Qi Zhang, Yyu Kong, Xiao-Qian Bian, Ying Wang, Shu Li
Objective: To investigate the effects of bosutinib on the early stage of cerebral ischemia-reperfusion injury in rats. Methods: Forty Sprague-Dawley rats were randomly divided into four groups (random number method), 10 rats in each group; sham group (control group): only neck vessels were isolated without other treatments; MCAO (model group): the rat brain ischemia/reperfusion injury model was made by a modified wire bolus method,ischemia for 2 h followed by reperfusion for 24 h; DMSO group (solvent group): DMSO ( 0.752 ml/kg) was injected into the tail vein one day before the experiment, brain ischemia 2 h reperfusion for 24 h; Bosutinib group (intervention group): one day before the experiment, the tail vein was injected with Bosutinib (4 mg/kg), brain ischemia 2 h reperfusion for 24 h. After 24 h of ischemia reperfusion, neurological function score was performed; brain infarct area was calculated after staining with TTC; SIK2 was detected by Western blot; the contents of TNF-α and IL-6 in brain tissue were detected by ELISA. Results: Compared with the sham group, the neurological function scores, the infarct volume percentages and the levels of inflammatory factors IL-6 and TNF-α of the MCAO and DMSO groups were increased significantly (P＜0.05 or P＜0.01). Compared with the MCAO and DMSO groups, the above mentioned indexes of the bosutinib group were all decreased significantly (P＜0.05 or P＜ 0.01). Compared with sham group, the expression levels of SIK2 protein in MCAO and DMSO groups had no significant changes(P＞ 0.05); compared with the MCAO and DMSO group, the expression level of SIK2 protein in the bosutinib group was decreased significantly (P＜0.05). Conclusion: Bosutinib reduces cerebral ischemia-reperfusion-induced injury, and its possible mechanism is related to the decreased expression of SIK2 protein and inflammatory factors.
{"title":"[Effects of Bosutinib on cerebral ischemia/reperfusion injury in rats].","authors":"Yi Zhang, Chao Wu, Qi Zhang, Yyu Kong, Xiao-Qian Bian, Ying Wang, Shu Li","doi":"10.12047/j.cjap.6327.2022.146","DOIUrl":"https://doi.org/10.12047/j.cjap.6327.2022.146","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects of bosutinib on the early stage of cerebral ischemia-reperfusion injury in rats. <b>Methods:</b> Forty Sprague-Dawley rats were randomly divided into four groups (random number method), 10 rats in each group; sham group (control group): only neck vessels were isolated without other treatments; MCAO (model group): the rat brain ischemia/reperfusion injury model was made by a modified wire bolus method,ischemia for 2 h followed by reperfusion for 24 h; DMSO group (solvent group): DMSO ( 0.752 ml/kg) was injected into the tail vein one day before the experiment, brain ischemia 2 h reperfusion for 24 h; Bosutinib group (intervention group): one day before the experiment, the tail vein was injected with Bosutinib (4 mg/kg), brain ischemia 2 h reperfusion for 24 h. After 24 h of ischemia reperfusion, neurological function score was performed; brain infarct area was calculated after staining with TTC; SIK2 was detected by Western blot; the contents of TNF-α and IL-6 in brain tissue were detected by ELISA. <b>Results:</b> Compared with the sham group, the neurological function scores, the infarct volume percentages and the levels of inflammatory factors IL-6 and TNF-α of the MCAO and DMSO groups were increased significantly (<i>P</i>＜0.05 or <i>P</i>＜0.01). Compared with the MCAO and DMSO groups, the above mentioned indexes of the bosutinib group were all decreased significantly (<i>P</i>＜0.05 or <i>P</i>＜ 0.01). Compared with sham group, the expression levels of SIK2 protein in MCAO and DMSO groups had no significant changes(<i>P</i>＞ 0.05); compared with the MCAO and DMSO group, the expression level of SIK2 protein in the bosutinib group was decreased significantly (<i>P</i>＜0.05). <b>Conclusion:</b> Bosutinib reduces cerebral ischemia-reperfusion-induced injury, and its possible mechanism is related to the decreased expression of SIK2 protein and inflammatory factors.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"803-806"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9618061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: Three modeling methods were used to establish a mouse primary liver cancer model, and compared them to find a more optimal modeling method. Methods: Forty 15-day-old C3H/HeN male mice were randomly divided into groups I-IV, 10 mice in each group. Group Ⅰ were not treated; Group Ⅱ were intraperitoneally injected with 25 mg/kg diethylnitrosamine (DEN) once; Group Ⅲ were intraperitoneally injected with 100 mg/kg DEN once; Group Ⅳ were intraperitoneally injected with 25 mg/kg DEN once and followed by another intraperitoneal injection of 100 mg/kg DEN at 42 days of age. The mortality of mice in each group was analyzed. At the 18th week of modeling, blood was collected from eyeballs after anesthesia, and liver was taken from abdominal cavity after neck was broken. The appearance of liver, the number of cancer nodules and the incidence of liver tumor were observed. The histopathological changes of liver were observed by HE staining. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. Results: At the 18th week of modeling, compared with the group I, serum levels of ALT and AST in groups II-IV were increased significantly (P＜0.05); The number of cancer nodules and the incidence of tumors in the surviving mice of groups III and IV were also increased significantly (P＜0.05). At the 18th week of modeling, no mice died in both groups I and II, and the incidence of liver cancer was 0%; The incidence of liver cancer in surviving mice in both groups III and IV was 100%, but the mortality rate of mice in group III was as high as 50%, and that in group IV was only 20%. Conclusion: C3H/HeN male mice can successfully establish a mouse liver cancer model by intraperitoneal injection of 25 mg/kg of DEN once at the age of 15 days and another intraperitoneal injection of 100 mg/kg of DEN once at the age of 42 days with short cycle and low mortality, which is an ideal method to establish a primary liver cancer model.
{"title":"[Establishment of primary liver cancer model in mice].","authors":"Jin-Jin Wang, Xue-Ying Li, Jin-Ke Yi, Bei-Ling Zhao, Hui-Min Huang, Ying Wei","doi":"10.12047/j.cjap.6367.2022.149","DOIUrl":"https://doi.org/10.12047/j.cjap.6367.2022.149","url":null,"abstract":"<p><p><b>Objective:</b> Three modeling methods were used to establish a mouse primary liver cancer model, and compared them to find a more optimal modeling method. <b>Methods:</b> Forty 15-day-old C3H/HeN male mice were randomly divided into groups I-IV, 10 mice in each group. Group Ⅰ were not treated; Group Ⅱ were intraperitoneally injected with 25 mg/kg diethylnitrosamine (DEN) once; Group Ⅲ were intraperitoneally injected with 100 mg/kg DEN once; Group Ⅳ were intraperitoneally injected with 25 mg/kg DEN once and followed by another intraperitoneal injection of 100 mg/kg DEN at 42 days of age. The mortality of mice in each group was analyzed. At the 18th week of modeling, blood was collected from eyeballs after anesthesia, and liver was taken from abdominal cavity after neck was broken. The appearance of liver, the number of cancer nodules and the incidence of liver tumor were observed. The histopathological changes of liver were observed by HE staining. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. <b>Results:</b> At the 18th week of modeling, compared with the group I, serum levels of ALT and AST in groups II-IV were increased significantly (<i>P</i>＜0.05); The number of cancer nodules and the incidence of tumors in the surviving mice of groups III and IV were also increased significantly (<i>P</i>＜0.05). At the 18th week of modeling, no mice died in both groups I and II, and the incidence of liver cancer was 0%; The incidence of liver cancer in surviving mice in both groups III and IV was 100%, but the mortality rate of mice in group III was as high as 50%, and that in group IV was only 20%. <b>Conclusion:</b> C3H/HeN male mice can successfully establish a mouse liver cancer model by intraperitoneal injection of 25 mg/kg of DEN once at the age of 15 days and another intraperitoneal injection of 100 mg/kg of DEN once at the age of 42 days with short cycle and low mortality, which is an ideal method to establish a primary liver cancer model.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"820-823"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9624122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.12047/j.cjap.6359.2022.124
Qi-Long Zhang, Jing Qu, Xiao-Hui Wang
Objective: To investigate the effects of adipokines chemerin on the improvement of islet function caused by exercise in mice with diabetes, and the possible mechanism of glucagon-like peptide 1 (GLP-1). Methods: Male ICR mice were randomly divided into a control group fed with normal diet (Con, n=6) and a diabetic modeling group fed with 60% kcal high-fat diet (n=44). After 6 weeks, the diabetic modeling group was once given a fasting intraperitoneal injection of streptozotocin (100 mg/kg). The successfully modeled mice were divided into diabetes group (DM), diabetes plus exercise group (EDM), and diabetes plus exercise and exogenous chemerin group (EDMC), 6 in each group. Mice in exercise groups participated in a six-week modest intensity treadmill running exercise with a gradually increased load. Mice in the EDMC group were intraperitoneally injected with exogenous chemerin (8 μg/kg) from the 4th week of the exercise period, six days per week, and one time per day. And the other groups were untreated. Adipose chemerin knockout mice were constructed. Then they and the control mice were divided into 6 groups (n=4): Normal diet control group (Con-ND), Normal diet chemerin knockout heterozygote mice group (Chemerin(+/-)-ND), Normal diet chemerin knockout homozygotes mice group(Chemerin(-/-)-ND), High-fat diet control group (Con-HFD), High-fat diet chemerin knockout heterozygote mice group (Chemerin(+/-)-HFD), High-fat diet chemerin knockout homozygotes mice group (Chemerin(-/-)-HFD). They were fed with normal or high-fat diet for 11 weeks and oral glucose tolerance test (OGTT) was conducted. After the mice of each group were executed under anesthesia, the samples such as pancreas and colon were collected. Fasting blood glucose (FBG) and fasting insulin (FINS) levels in mice were measured, and the insulin resistance index (HOMA-IR) was calculated. HE staining was used to observe the structure of islets. ELISA was used to detect the GLP-1 level in serum. The mRNA levels of proglucagon (GCG) and chemerin in the colon were measured by real-time PCR. And the protein levels of GCG and chemerin in the colon were detected by Western blot. Results: Compared with the DM group, the vacuolar degeneration and shrinkage of islet cells in the EDM group were reduced, the islet structure was improved, while the levels of FINS, HOMA-IR and FBG were decreased significantly (P＜0.05 or P＜0.01). The colon and serum chemerin levels were decreased significantly(P＜0.05), while the colonic GCG mRNA and protein levels were increased significantly (P＜0.05 or P＜0.01). Compared with the EDM group, the islet cells in the EDMC group were shrunken, with unclear borders. The structure of the islets was damaged, and the levels of FINS, HOMA-IR and FBG were increased significantly (P＜0.01), while the mRNA and protein levels of GCG were decreased significantly (P＜0.05 or P＜0.01). Co
{"title":"[Effects of adipokine chemerin on the improvement of islet function in diabetic mice by aerobic exercise and its mechanisms].","authors":"Qi-Long Zhang, Jing Qu, Xiao-Hui Wang","doi":"10.12047/j.cjap.6359.2022.124","DOIUrl":"https://doi.org/10.12047/j.cjap.6359.2022.124","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects of adipokines chemerin on the improvement of islet function caused by exercise in mice with diabetes, and the possible mechanism of glucagon-like peptide 1 (GLP-1). <b>Methods:</b> Male ICR mice were randomly divided into a control group fed with normal diet (Con, <i>n</i>=6) and a diabetic modeling group fed with 60% kcal high-fat diet (<i>n</i>=44). After 6 weeks, the diabetic modeling group was once given a fasting intraperitoneal injection of streptozotocin (100 mg/kg). The successfully modeled mice were divided into diabetes group (DM), diabetes plus exercise group (EDM), and diabetes plus exercise and exogenous chemerin group (EDMC), 6 in each group. Mice in exercise groups participated in a six-week modest intensity treadmill running exercise with a gradually increased load. Mice in the EDMC group were intraperitoneally injected with exogenous chemerin (8 μg/kg) from the 4th week of the exercise period, six days per week, and one time per day. And the other groups were untreated. Adipose chemerin knockout mice were constructed. Then they and the control mice were divided into 6 groups (<i>n</i>=4): Normal diet control group (Con-ND), Normal diet chemerin knockout heterozygote mice group (Chemerin(+/-)-ND), Normal diet chemerin knockout homozygotes mice group(Chemerin(-/-)-ND), High-fat diet control group (Con-HFD), High-fat diet chemerin knockout heterozygote mice group (Chemerin(+/-)-HFD), High-fat diet chemerin knockout homozygotes mice group (Chemerin(-/-)-HFD). They were fed with normal or high-fat diet for 11 weeks and oral glucose tolerance test (OGTT) was conducted. After the mice of each group were executed under anesthesia, the samples such as pancreas and colon were collected. Fasting blood glucose (FBG) and fasting insulin (FINS) levels in mice were measured, and the insulin resistance index (HOMA-IR) was calculated. HE staining was used to observe the structure of islets. ELISA was used to detect the GLP-1 level in serum. The mRNA levels of proglucagon (GCG) and chemerin in the colon were measured by real-time PCR. And the protein levels of GCG and chemerin in the colon were detected by Western blot. <b>Results:</b> Compared with the DM group, the vacuolar degeneration and shrinkage of islet cells in the EDM group were reduced, the islet structure was improved, while the levels of FINS, HOMA-IR and FBG were decreased significantly (<i>P</i>＜0.05 or <i>P</i>＜0.01). The colon and serum chemerin levels were decreased significantly(<i>P</i>＜0.05), while the colonic GCG mRNA and protein levels were increased significantly (<i>P</i>＜0.05 or <i>P</i>＜0.01). Compared with the EDM group, the islet cells in the EDMC group were shrunken, with unclear borders. The structure of the islets was damaged, and the levels of FINS, HOMA-IR and FBG were increased significantly (<i>P</i>＜0.01), while the mRNA and protein levels of GCG were decreased significantly (<i>P</i>＜0.05 or <i>P</i>＜0.01). Co","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"682-689"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9629794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.12047/j.cjap.6374.2022.137
Qing-Ya Zhuo, He Qian, Bao-Sheng Zhao, Bo Qi, Yu-Zhen Liu
Objective: To investigate the effects of propranolol on the subcutaneous tumorigenesis of esophageal squamous cell carcinoma (ESCC) cells and the proliferation, migration, cell cycle, apoptosis and autophagy of ESCC cells and its possible molecular mechanisms. Methods: The cell proliferation was detected by MTT (methyl thiazol tetrazolium) assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured. PBS (Phosphate buffer saline) group (without propranolol) and treated groups (40, 60, 80, 100 μmol/L propranolol) were set up with 5 wells in each group. After treatment for 0, 24, 48, 72 h, 10 μl (5 mg/ml) of MTT was added to each well, and the absorbance was measured at 490 nm. The cell migration was tested by Transwell assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured, and PBS group (without propranolol) and treated groups (40, 60 μmol/L) were set up with 2 wells in each group. Photos were taken 40 h later, and the experiment was repeated for three times before statistical analysis. The cell cycle and apoptosis were detected by flow cytometry assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured. PBS group (without propranolol) and treated group (80 μmol/L) were set up, fixed, stained, and fluorescence at 488 nm was detected. The protein levels were detected by Western blot: ESCC Eca109 and KYSE-450 cells were routinely cultured. PBS group (without propranolol) and treated groups (60, 80 μmol/L) were set up followed by gel electrophoresis, wet membrane transfer, and ECL imaging. The experiment was repeated for three times and then analyzed statistically. Subcutaneous tumor formation experiment in nude mice: 10 nude mice were assigned PBS group (without propranolol) and treated group (with propranolol). Five mice in each group were inoculated with 5×106 cells/100 μl (Eca109) into the right underarm. The treated group was given a gavage of 0.4 ml/kg (6 mg/kg) every other day, and the tumor size was measured every other day for 3 weeks. After 20 days, the nude mice were dislocated and sacrificed to take tumor tissue. Result: The results showed that propranolol inhibited the proliferation of Eca109, KYSE-450 and TE-1 cells with IC50 of around 70 μmol/L for 48 h. Eca109, KYSE-450 and TE-1 cell migration was inhibited by propranolol in a dose-dependent manner (P＜0.05); Propranolol blocked the cell cycle of Eca109 in G2/M phase, blocked the cell cycle of KYSE-450 and TE-1 in G0/G1 phase, and promoted apoptosis of three kinds of cells (P＜0.05). The results of cell fluorescence showed that LC3 fluorescence intensity of TE-1 was increased after 12 h, 24 h and 36 h treatment with propranolol (P＜0.05). Western blot results showed that compared with PBS group, the protein expressions of p-mTOR, p-Akt and cyclin D1 were down-regulated, while cleaved caspase 9 level was up-regulated (P＜0.05). The results of subcutaneous tumor formation in nude mice showed that the tumor weight of PBS group was (0.91±0.05)g, and that of the
{"title":"[Effects of propranolol on biological function of human esophageal squamous cell carcinoma cells].","authors":"Qing-Ya Zhuo, He Qian, Bao-Sheng Zhao, Bo Qi, Yu-Zhen Liu","doi":"10.12047/j.cjap.6374.2022.137","DOIUrl":"https://doi.org/10.12047/j.cjap.6374.2022.137","url":null,"abstract":"Objective: To investigate the effects of propranolol on the subcutaneous tumorigenesis of esophageal squamous cell carcinoma (ESCC) cells and the proliferation, migration, cell cycle, apoptosis and autophagy of ESCC cells and its possible molecular mechanisms. Methods: The cell proliferation was detected by MTT (methyl thiazol tetrazolium) assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured. PBS (Phosphate buffer saline) group (without propranolol) and treated groups (40, 60, 80, 100 μmol/L propranolol) were set up with 5 wells in each group. After treatment for 0, 24, 48, 72 h, 10 μl (5 mg/ml) of MTT was added to each well, and the absorbance was measured at 490 nm. The cell migration was tested by Transwell assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured, and PBS group (without propranolol) and treated groups (40, 60 μmol/L) were set up with 2 wells in each group. Photos were taken 40 h later, and the experiment was repeated for three times before statistical analysis. The cell cycle and apoptosis were detected by flow cytometry assay: ESCC Eca109, KYSE-450 and TE-1 cells were routinely cultured. PBS group (without propranolol) and treated group (80 μmol/L) were set up, fixed, stained, and fluorescence at 488 nm was detected. The protein levels were detected by Western blot: ESCC Eca109 and KYSE-450 cells were routinely cultured. PBS group (without propranolol) and treated groups (60, 80 μmol/L) were set up followed by gel electrophoresis, wet membrane transfer, and ECL imaging. The experiment was repeated for three times and then analyzed statistically. Subcutaneous tumor formation experiment in nude mice: 10 nude mice were assigned PBS group (without propranolol) and treated group (with propranolol). Five mice in each group were inoculated with 5×106 cells/100 μl (Eca109) into the right underarm. The treated group was given a gavage of 0.4 ml/kg (6 mg/kg) every other day, and the tumor size was measured every other day for 3 weeks. After 20 days, the nude mice were dislocated and sacrificed to take tumor tissue. Result: The results showed that propranolol inhibited the proliferation of Eca109, KYSE-450 and TE-1 cells with IC50 of around 70 μmol/L for 48 h. Eca109, KYSE-450 and TE-1 cell migration was inhibited by propranolol in a dose-dependent manner (P＜0.05); Propranolol blocked the cell cycle of Eca109 in G2/M phase, blocked the cell cycle of KYSE-450 and TE-1 in G0/G1 phase, and promoted apoptosis of three kinds of cells (P＜0.05). The results of cell fluorescence showed that LC3 fluorescence intensity of TE-1 was increased after 12 h, 24 h and 36 h treatment with propranolol (P＜0.05). Western blot results showed that compared with PBS group, the protein expressions of p-mTOR, p-Akt and cyclin D1 were down-regulated, while cleaved caspase 9 level was up-regulated (P＜0.05). The results of subcutaneous tumor formation in nude mice showed that the tumor weight of PBS group was (0.91±0.05)g, and that of the ","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"754-759"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9618062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Effects of Danzhen headache capsule on the expression of CREB and ERK in CM rats by mediated central sensitization mechanism].","authors":"Rui-Qiong Wang, Yan-Mei Ning, Guo-Tai Wu, Li-Dong DU, Zhi-Wang Wang","doi":"10.12047/j.cjap.6329.2022.140","DOIUrl":"https://doi.org/10.12047/j.cjap.6329.2022.140","url":null,"abstract":"目的: 探讨丹珍头痛胶囊对中枢敏感介导的慢性偏头痛大鼠的干预作用。方法: 将60只SD大鼠随机分为正常组、模型组、盐酸氟桂利嗪组(FNZ)、丹珍头痛胶囊(DZTT)高、中、低剂量组(1.0、0.5、0.25 g/kg)(n=10)。采用连续皮下注射硝酸甘油法制作慢性偏头痛大鼠模型,丹珍头痛胶囊给予大鼠灌胃治疗,每天1次,连续35 d。观测各组大鼠大体状态、耳红出现及消失时间、搔头次数、爬笼次数等疼痛行为学指标,测定眶周及足底的机械痛阈值,RT-PCR及Western blot技术分别检测三叉神经脊束核尾侧(TNC)组织中CREB、ERK的mRNA表达及CREB、pCREB、ERK、pERK蛋白表达水平。结果: 与正常组比较,模型组大鼠行为学评分明显升高,眶周及足底机械痛阈值逐日下降,TNC组织中CREB、ERK基因表达及CREB、pCREB、ERK、pERK蛋白表达水平均显著升高(P＜0.01);与模型组比较,DZTT、FNZ组大鼠疼痛症状明显缓解,疼痛行为学评分显著降低而眶周及足底机械痛阈值显著升高,TNC组织中CREB、ERK基因表达及CREB、pCREB、ERK、pERK蛋白表达水平均显著下降(P＜0.05,P＜0.01);与FNZ组比较,在给药第35日,DZTT高剂量组大鼠疼痛行为学评分、眶周及足底机械痛阈、TNC组织中CREB mRNA表达及ERK、pERK蛋白表达水平差异无显著性(P＞0.05)。结论: DZTT对中枢敏感介导的慢性偏头痛具有一定的治疗作用,抑制CREB、ERK的激活和磷酸化是其可能机制之一。.","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"771-775"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9629800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.12047/j.cjap.6356.2022.110
Ying Zhao, Hai Wang
Objective: To investigate the interventional effects of a new SUR2B/Kir6.1-type KATP Channel opener iptakalim on injury renal cells (the renal glomerular endothelial, mesangial and tubular epithelial cells) and its mechanisms. Methods: ①Experimental protocol: control: the cells were treated with with 0 mg/L uric acid for 24 h; model: the cells were treated with with 1 200 mg/L uric acid for 24 h; pretreatment with iptakalim: the cells were pretreated with 0.01,0.1,1,10,100 μmol/L iptakalim for 24 h prior to treatment with 1 200 mg/L uric acid for 24 h; pretreatment with glibenclamide: the cells were preincubated with/without 10 μmol/L glibenclamide for 1 h and then treated with 10 μmol/L iptakalim for 24 h followed by incubation with 1 200 mg/L uric acid for another 24 h. ②The cell viability was measured by MTT assay and flow cytometry; the protein expressions of Kir6.1 and SUR2B and nuclear translocation were detected by immunostaining; the protein expressions of Kir6.1 and SUR2B were determined by Western blot analysis; adhesion of mononuclear cells to endothelial cells were tested by fluorimetric assay; the content of MCP-1 was measured by enzyme linked-immunosorbent assay (ELISA). Results: The renal glomerular endothelial, mesangial and tubular epithelial cells were exposed to 1 200 mg/L uric acid for 24 h. Compared with the control group, 1 200 mg/L uric acid decreased the cell survival rates significantly (P＜0.01, P＜0.01, P＜0.01). Compared with the model group, pretreatment with 0.1, 1, 10, 100 μmol/L iptakalim could remarkably alleviate cellular damages of glomerular endothelium, mesangium cells induced by uric acid (P＜0.05, P＜0.01, P＜0.01, P＜0.01). The KATP channel blocker could clearly reduce survival rates of the renal glomerular endothelial, mesangial cells(P＜0.01) and markedly reverse the inhibitory effects of iptakalim on cell death (P＜0.05, P＜0.01), no obvious difference in comparison with the model group (P＞0.05). Compared with the model group, pretreatment with 10, 100 μmol/L iptakalim could notably attenuate cellular damages of tubular epithelial cells induced by uric acid (P＜0.05, P＜0.05). The KATP channel blocker could obviously damage the tubular epithelial cells (P＜0.01), no obvious difference in comparison with the model group (P＞0.05). Compared with control group, exposure of renal tubular epithelial, mesangial and glomerular endothelial cells to 1 200 mg/L uric acid for 24 h caused a significant increase in the protein expressions of Kir6.1 and SUR2B(P＜0.05). Compared with the model group, the overexpressions of Kir6.1 and SUR2B were suppressed in presence of iptakalim at a concentration of 10 μmol/L (P＜0.05). These decreases in the expressions of Kir6.1 and SUR2B were prevented by the KATP channel blocker, no obvious difference in comp
{"title":"[Interventional effects of activating SUR2B/Kir6.1-type K<sub>ATP</sub> channels on renal cells injury and its mechanisms].","authors":"Ying Zhao, Hai Wang","doi":"10.12047/j.cjap.6356.2022.110","DOIUrl":"https://doi.org/10.12047/j.cjap.6356.2022.110","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the interventional effects of a new SUR2B/Kir6.1-type K<sub>ATP</sub> Channel opener iptakalim on injury renal cells (the renal glomerular endothelial, mesangial and tubular epithelial cells) and its mechanisms. <b>Methods:</b> ①Experimental protocol: control: the cells were treated with with 0 mg/L uric acid for 24 h; model: the cells were treated with with 1 200 mg/L uric acid for 24 h; pretreatment with iptakalim: the cells were pretreated with 0.01,0.1,1,10,100 μmol/L iptakalim for 24 h prior to treatment with 1 200 mg/L uric acid for 24 h; pretreatment with glibenclamide: the cells were preincubated with/without 10 μmol/L glibenclamide for 1 h and then treated with 10 μmol/L iptakalim for 24 h followed by incubation with 1 200 mg/L uric acid for another 24 h. ②The cell viability was measured by MTT assay and flow cytometry; the protein expressions of Kir6.1 and SUR2B and nuclear translocation were detected by immunostaining; the protein expressions of Kir6.1 and SUR2B were determined by Western blot analysis; adhesion of mononuclear cells to endothelial cells were tested by fluorimetric assay; the content of MCP-1 was measured by enzyme linked-immunosorbent assay (ELISA). <b>Results:</b> The renal glomerular endothelial, mesangial and tubular epithelial cells were exposed to 1 200 mg/L uric acid for 24 h. Compared with the control group, 1 200 mg/L uric acid decreased the cell survival rates significantly (<i>P</i>＜0.01, <i>P</i>＜0.01, <i>P</i>＜0.01). Compared with the model group, pretreatment with 0.1, 1, 10, 100 μmol/L iptakalim could remarkably alleviate cellular damages of glomerular endothelium, mesangium cells induced by uric acid (<i>P</i>＜0.05, <i>P</i>＜0.01, <i>P</i>＜0.01, <i>P</i>＜0.01). The K<sub>ATP</sub> channel blocker could clearly reduce survival rates of the renal glomerular endothelial, mesangial cells(<i>P</i>＜0.01) and markedly reverse the inhibitory effects of iptakalim on cell death (<i>P</i>＜0.05, <i>P</i>＜0.01), no obvious difference in comparison with the model group (<i>P</i>＞0.05). Compared with the model group, pretreatment with 10, 100 μmol/L iptakalim could notably attenuate cellular damages of tubular epithelial cells induced by uric acid (<i>P</i>＜0.05, <i>P</i>＜0.05). The K<sub>ATP</sub> channel blocker could obviously damage the tubular epithelial cells (<i>P</i>＜0.01), no obvious difference in comparison with the model group (<i>P</i>＞0.05). Compared with control group, exposure of renal tubular epithelial, mesangial and glomerular endothelial cells to 1 200 mg/L uric acid for 24 h caused a significant increase in the protein expressions of Kir6.1 and SUR2B(<i>P</i>＜0.05). Compared with the model group, the overexpressions of Kir6.1 and SUR2B were suppressed in presence of iptakalim at a concentration of 10 μmol/L (<i>P</i>＜0.05). These decreases in the expressions of Kir6.1 and SUR2B were prevented by the K<sub>ATP</sub> channel blocker, no obvious difference in comp","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"604-610"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9680481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.12047/j.cjap.6351.2022.115
Xuan Liu, Hui-Peng Nie, Huan-Liang Liu, Yue Shi, Wen-Qing Lai, Zhu-Ge Xi, Ben-Cheng Lin
Objective: To investigate the effects of oil-mist particulate matter (OMPM) on cardiac tissue structure fibrosis in rats and the role of epithelial-mesenchymal transition (EMT). Methods: Six-week-old Wistar rats (half male and half female) were randomly divided into 3 groups: control group (without OMPM exposure), low-dose exposure group (50 mg/m3) and high-dose exposure group (100 mg/m3), 18 rats in each group, with 6.5 hours per day of dynamic inhalation exposure. After 42 days of continuous exposure, cardiac tissues were collected for morphological observation; Western blot was used to detect fibrosis markers collagen I and collagen III levels, epithelial marker E-cadherin levels, interstitial markers N-cadherin, fibronectin, vimentin, alpha-smooth muscle actin (α-SMA) levels, and EMT transcription factor Twist protein levels; Real-time polymerase chain reaction (RT-qPCR) was used to detect collagen I and collagen III mRNA levels. Results: After OMPM exposure, myocardial cell edema and collagen fiber deposition were increased gradually with increasing exposure dose. Western blot results showed that compared with the control group, the expression levels of collagen I, collagen III, N-Cadherin, fibronectin, vimentin, α-SMA, and Twist protein were increased significantly in the low-dose exposure group and the high-dose exposure group (P＜0.01), and protein expression levels were higher in the high-dose exposure group than those in the low-dose exposure group (P＜0.01). In contrast, E-Cadherin protein expression levels were decreased significantly, and lower in the high-dose exposure group (P＜0.01). RT-qPCR results showed that compared with the control group, collagen I and collagen III mRNA levels were increased significantly in the low-dose exposure group and the high-dose exposure group (P＜0.01), and were increased with increasing exposure dose. (P＜0.01). Conclusion: OMPM may induce cardiac fibrosis in rats by promoting EMT process.
{"title":"[Effect of epithelial-mesenchymal transition on cardiac fibrosis induced by oil mist particulate matter].","authors":"Xuan Liu, Hui-Peng Nie, Huan-Liang Liu, Yue Shi, Wen-Qing Lai, Zhu-Ge Xi, Ben-Cheng Lin","doi":"10.12047/j.cjap.6351.2022.115","DOIUrl":"https://doi.org/10.12047/j.cjap.6351.2022.115","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects of oil-mist particulate matter (OMPM) on cardiac tissue structure fibrosis in rats and the role of epithelial-mesenchymal transition (EMT). <b>Methods:</b> Six-week-old Wistar rats (half male and half female) were randomly divided into 3 groups: control group (without OMPM exposure), low-dose exposure group (50 mg/m<sup>3</sup>) and high-dose exposure group (100 mg/m<sup>3</sup>), 18 rats in each group, with 6.5 hours per day of dynamic inhalation exposure. After 42 days of continuous exposure, cardiac tissues were collected for morphological observation; Western blot was used to detect fibrosis markers collagen I and collagen III levels, epithelial marker E-cadherin levels, interstitial markers N-cadherin, fibronectin, vimentin, alpha-smooth muscle actin (α-SMA) levels, and EMT transcription factor Twist protein levels; Real-time polymerase chain reaction (RT-qPCR) was used to detect collagen I and collagen III mRNA levels. <b>Results:</b> After OMPM exposure, myocardial cell edema and collagen fiber deposition were increased gradually with increasing exposure dose. Western blot results showed that compared with the control group, the expression levels of collagen I, collagen III, N-Cadherin, fibronectin, vimentin, α-SMA, and Twist protein were increased significantly in the low-dose exposure group and the high-dose exposure group (<i>P</i>＜0.01), and protein expression levels were higher in the high-dose exposure group than those in the low-dose exposure group (<i>P</i>＜0.01). In contrast, E-Cadherin protein expression levels were decreased significantly, and lower in the high-dose exposure group (<i>P</i>＜0.01). RT-qPCR results showed that compared with the control group, collagen I and collagen III mRNA levels were increased significantly in the low-dose exposure group and the high-dose exposure group (<i>P</i>＜0.01), and were increased with increasing exposure dose. (<i>P</i>＜0.01). <b>Conclusion:</b> OMPM may induce cardiac fibrosis in rats by promoting EMT process.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"633-637"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9680485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate the effects and its mechanisms of silence information regulator 7(SIRT7)on mouse renal podocytes proliferation and apoptosis under high glucose environment. Methods: Mouse renal podocytes cultured with high glucose and treated with different methods were divided into the following groups:control group(Control),high glucose group(HG),high glucose+transfecting with SIRT7 overexpression vetor(pcDNA3.1-SIRT7) group(SIRT7 OE+HG),high glucose+transfecting with the negative control vetor(pcDNA3.1)group(SIRT7 OE-NC+HG),high glucose+transfecting with small interfering RNA-SIRT7 (siRNA-SIRT7) group (siRNA-SIRT7+HG), high glucose+ transfecting with siRNA-SIRT7 control group (siRNA-SIRT7-NC+ HG). Viability of proliferation was examined by CCK-8 method.Rate of apoptosis was detected by flow cytometry. The level of SIRT7 mRNA expression was measured by qRT-PCR. Western blot was performed to detect the protein expression of Nephrin and key factors of Wnt/β-catenin signaling pathway. Results: The CCK-8 result showed that,compared with control group, the proliferative activity of mouse renal podocytes in HG group was decreased (P＜0.05). After transfected with SIRT7 overexpression vetor or small interfering RNA-SIRT7,compared to HG group,the cell proliferation activity was further decreased in siRNA-SIRT7 group(P＜0.05),but it was enhanced in SIRT7 OE+HG group (P＜0.05). The results of flow cytometry showed that compared with the control group, the apoptosis rate of cells in the HG group was increased (P＜0.05). Compared with the HG group, the apoptosis rate of cells in the siRNA SIRT7+HG group was increased significantly(P＜0.05), while that in the SIRT7 OE+HG group was decreased (P＜0.05). Compared with control group,the expressions of Nephrin, Wnt5a and β-catenin were inhibited in HG group (P＜0.05). compared to HG group,siRNA-SIRT7 could down-regulate the expression levels of Nephrin, Wnt5a and β-catenin in siRNA-SIRT7 group (P＜0.05), SIRT7 overexpression could up-regulate the expression levels of Nephrin, Wnt5a and β-catenin in SIRT7 OE+HG group (P＜0.05). Conclusion: The findings suggest that high glucose environment is an important factor to inhibit the proliferation and induce apoptosis of mouse renal podocytes.Overexpression of SIRT7 can reverse the effects by activating Wnt/β-catenin signaling pathway and up-regulating β-catenin expression.
{"title":"[Effects of silence information regulator 7 on proliferation and apoptosis of mouse renal podocytes under high glucose environment].","authors":"Min Feng, Ting Lin, Xia-Xia Chen, Xiao-Ling Yang, Qi Lyu, Jun-Ping Wen","doi":"10.12047/j.cjap.6366.2022.111","DOIUrl":"https://doi.org/10.12047/j.cjap.6366.2022.111","url":null,"abstract":"<p><p><b>Objective:</b> To investigate the effects and its mechanisms of silence information regulator 7(SIRT7)on mouse renal podocytes proliferation and apoptosis under high glucose environment. <b>Methods:</b> Mouse renal podocytes cultured with high glucose and treated with different methods were divided into the following groups:control group(Control),high glucose group(HG),high glucose+transfecting with SIRT7 overexpression vetor(pcDNA3.1-SIRT7) group(SIRT7 OE+HG),high glucose+transfecting with the negative control vetor(pcDNA3.1)group(SIRT7 OE-NC+HG),high glucose+transfecting with small interfering RNA-SIRT7 (siRNA-SIRT7) group (siRNA-SIRT7+HG), high glucose+ transfecting with siRNA-SIRT7 control group (siRNA-SIRT7-NC+ HG). Viability of proliferation was examined by CCK-8 method.Rate of apoptosis was detected by flow cytometry. The level of SIRT7 mRNA expression was measured by qRT-PCR. Western blot was performed to detect the protein expression of Nephrin and key factors of Wnt/β-catenin signaling pathway. <b>Results:</b> The CCK-8 result showed that,compared with control group, the proliferative activity of mouse renal podocytes in HG group was decreased (<i>P</i>＜0.05). After transfected with SIRT7 overexpression vetor or small interfering RNA-SIRT7,compared to HG group,the cell proliferation activity was further decreased in siRNA-SIRT7 group(<i>P</i>＜0.05),but it was enhanced in SIRT7 OE+HG group (<i>P</i>＜0.05). The results of flow cytometry showed that compared with the control group, the apoptosis rate of cells in the HG group was increased (<i>P</i>＜0.05). Compared with the HG group, the apoptosis rate of cells in the siRNA SIRT7+HG group was increased significantly(<i>P</i>＜0.05), while that in the SIRT7 OE+HG group was decreased (P＜0.05). Compared with control group,the expressions of Nephrin, Wnt5a and β-catenin were inhibited in HG group (<i>P</i>＜0.05). compared to HG group,siRNA-SIRT7 could down-regulate the expression levels of Nephrin, Wnt5a and β-catenin in siRNA-SIRT7 group (<i>P</i>＜0.05), SIRT7 overexpression could up-regulate the expression levels of Nephrin, Wnt5a and β-catenin in SIRT7 OE+HG group (<i>P</i>＜0.05). <b>Conclusion:</b> The findings suggest that high glucose environment is an important factor to inhibit the proliferation and induce apoptosis of mouse renal podocytes.Overexpression of SIRT7 can reverse the effects by activating Wnt/β-catenin signaling pathway and up-regulating β-catenin expression.</p>","PeriodicalId":23985,"journal":{"name":"Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology","volume":"38 6","pages":"611-616"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10519353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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