Exposure of naive murine CD4 + T lymphocytes to superantigen such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell ...Exposure of naive murine CD4 + T lymphocytes to superantigen such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell population with SEB leads to the apoptotic events of activation-induced cell death (AICD). The signaling mechanism responsible for the AICD is a target of intensive investigation. However, the precise downstream signaling pathways of SEB-induced AICD remains unclear. Our results here show that the sequential activation of caspase-1/ICE-like and caspase-3/CPP32-like cysteine proteases probably plays a role in the signaling transduction of SEB-induced AICD, but caspase-3/CPP32-like proteases activation does not depend on caspase-1-like proteases activation. Herbimycin A, a specific inhibitor of protein tyrosine kinases, inhibit caspase-3/CPP32-like cysteine proteases activation. However, it does not prevent DNA fragmentation of CD4 + T cells apoptosis induced by SEB. These results indicate that protein tyrosine kinases pathway is probably involved in the signaling transduction of CD4 + T cells apoptosis induced by SEB and “crosstalks” with the pathway of caspase-3/CPP32-like proteases activation.展开更多
目的观察肝缺血再灌注不同时限中胰岛素样生长因子-Ⅰ(IGF-Ⅰ)及细胞凋亡蛋白酶-3(Caspase-3)的表达特点并探讨IGF-Ⅰ与肝脏功能及细胞凋亡的关系。方法75只大鼠分为正常对照组、假手术组及缺血再灌注组,每组25只。采用免疫组化方法检测...目的观察肝缺血再灌注不同时限中胰岛素样生长因子-Ⅰ(IGF-Ⅰ)及细胞凋亡蛋白酶-3(Caspase-3)的表达特点并探讨IGF-Ⅰ与肝脏功能及细胞凋亡的关系。方法75只大鼠分为正常对照组、假手术组及缺血再灌注组,每组25只。采用免疫组化方法检测IGF-Ⅰ及Caspase-3的表达,并采用全自动生化仪检测AST、ALT水平,以光学显微镜及电子显微镜观察组织形态学变化。结果肝缺血45 min再灌注后IGF-Ⅰ表达水平在再灌注3、12、24 h 3组降低,与同期对照组和假手术组差异有统计学意义(P<0.01),不同肝组织结构表达水平亦不同。Caspase-3缺血45min再灌注3h时表达开始增多,在24h组表达水平最高,与对照组和假手术组差异有统计学意义(P<0.01),至72h表达水平接近于正常组(P>0.05)。外周血清AST、ALT浓度在再灌注后0、3、12、24h较同期正常对照及假手术组高(P<0.01),72min接近正常。结论IGF-Ⅰ可以作为肝脏缺血再灌注时反映肝脏功能的一项指标,它在此期不同时限的表达具有空间特异性,并有可能对缺血再灌注损伤引发的细胞凋亡有拮抗作用。展开更多
Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to disc...Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to discuss the mechanism of EA in the treatment of DES from the perspective of cell apoptosis.Methods:Male New Zealand rabbits were randomly divided into a normal group(NG),a model group(MG),an EA group(EAG)and a sham EA group(SEAG).DES rabbit model was developed by eye drop of 0.1%benzalkonium chloride.The rabbit tear secretion and tear film break-up time(BUT)were measured;terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay was used to detect the apoptosis of conjunctival cells;the expressions of Caspase-3,Fas and Bcl-2 proteins in conjunctival cells were detected by immunohistochemistry.Results:Compared with the NG,the rabbit tear secretion decreased and the BUT was shortened in the MG(both P<0.01);compared with the MG and the SEAG,the rabbit tear secretion increased and the BUT was prolonged in the EAG(all P<0.05).Compared with the NG,the apoptosis of rabbit conjunctival cells increased(P<0.01),the expressions of Caspase-3 and Fas proteins increased(both P<0.05),and the expression of Bcl-2 protein decreased(P<0.01)in the MG;compared with the MG and the SEAG,the apoptosis of rabbit conjunctival cells decreased(both P<0.01),the expressions of Caspase-3 and Fas proteins decreased(all P<0.05),and the expression of Bcl-2 protein increased(both P<0.01)in the EAG.Conclusion:EA can inhibit the apoptosis of rabbit conjunctival cells,down-regulate the expressions of apoptosis-related proteins Caspase-3 and Fas,and up-regulate the expression of Bcl-2 protein,which may be one of the mechanisms of EA in treatment of DES.展开更多
We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneal y for 12 we...We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneal y for 12 weeks. Myocardial injury indices and oxidative stress markers were determined. Changes in cardiac ultrastructure were evaluated with transmission electron microscopy. Myocardial apoptosis was assessed via terminal deoxynucleotidyl transferase （TDT）-mediated DNA nick-end labeling （TUNEL） and immunohistochemistry. Ginsenoside Rg1 was as-sociated with a significant dose-dependent reduction in serum levels of creatinine kinase MB and cardiac troponin I, and lessened ultrastructural disorders in diabetic myocardium, relative to the untreated diabetic model rats. Also, compared with the untreated diabetic rats, significant reductions in serum and myocardial levels of malondialdehyde were noted in the ginsenoside Rg1-treated groups, and increased levels of the antioxidants （superoxide dismutase, catalase, and glutathione peroxidase） were detected. TUNEL staining indicated reduced myocardial apoptosis in ginsenoside Rg1-treated rats, which may be associated with reduced levels of caspase-3 （CASP3） and increased levels of B-cell lymphoma-extra-large （Bcl-xL） in the diabetic myocardium. Ginsenoside Rg1 treatment of diabetic rats was associated with reduced oxidative stress and attenuated myocardial apoptosis, suggesting that ginsenoside Rg1 may be of potential preventative and therapeutic value for cardiovascular injury in diabetic patients.展开更多
基金This study was supported by a grant from the Natural Science Foundation of China (No.30070703)
文摘Exposure of naive murine CD4 + T lymphocytes to superantigen such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell population with SEB leads to the apoptotic events of activation-induced cell death (AICD). The signaling mechanism responsible for the AICD is a target of intensive investigation. However, the precise downstream signaling pathways of SEB-induced AICD remains unclear. Our results here show that the sequential activation of caspase-1/ICE-like and caspase-3/CPP32-like cysteine proteases probably plays a role in the signaling transduction of SEB-induced AICD, but caspase-3/CPP32-like proteases activation does not depend on caspase-1-like proteases activation. Herbimycin A, a specific inhibitor of protein tyrosine kinases, inhibit caspase-3/CPP32-like cysteine proteases activation. However, it does not prevent DNA fragmentation of CD4 + T cells apoptosis induced by SEB. These results indicate that protein tyrosine kinases pathway is probably involved in the signaling transduction of CD4 + T cells apoptosis induced by SEB and “crosstalks” with the pathway of caspase-3/CPP32-like proteases activation.
文摘目的观察肝缺血再灌注不同时限中胰岛素样生长因子-Ⅰ(IGF-Ⅰ)及细胞凋亡蛋白酶-3(Caspase-3)的表达特点并探讨IGF-Ⅰ与肝脏功能及细胞凋亡的关系。方法75只大鼠分为正常对照组、假手术组及缺血再灌注组,每组25只。采用免疫组化方法检测IGF-Ⅰ及Caspase-3的表达,并采用全自动生化仪检测AST、ALT水平,以光学显微镜及电子显微镜观察组织形态学变化。结果肝缺血45 min再灌注后IGF-Ⅰ表达水平在再灌注3、12、24 h 3组降低,与同期对照组和假手术组差异有统计学意义(P<0.01),不同肝组织结构表达水平亦不同。Caspase-3缺血45min再灌注3h时表达开始增多,在24h组表达水平最高,与对照组和假手术组差异有统计学意义(P<0.01),至72h表达水平接近于正常组(P>0.05)。外周血清AST、ALT浓度在再灌注后0、3、12、24h较同期正常对照及假手术组高(P<0.01),72min接近正常。结论IGF-Ⅰ可以作为肝脏缺血再灌注时反映肝脏功能的一项指标,它在此期不同时限的表达具有空间特异性,并有可能对缺血再灌注损伤引发的细胞凋亡有拮抗作用。
文摘Objective:By observing the effects of electroacupuncture(EA)on the apoptosis of conjunctival cells of rabbits with dry eye syndrome(DES)and the expressions of apoptosis-related proteins Caspase-3,Fas and Bcl-2,to discuss the mechanism of EA in the treatment of DES from the perspective of cell apoptosis.Methods:Male New Zealand rabbits were randomly divided into a normal group(NG),a model group(MG),an EA group(EAG)and a sham EA group(SEAG).DES rabbit model was developed by eye drop of 0.1%benzalkonium chloride.The rabbit tear secretion and tear film break-up time(BUT)were measured;terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay was used to detect the apoptosis of conjunctival cells;the expressions of Caspase-3,Fas and Bcl-2 proteins in conjunctival cells were detected by immunohistochemistry.Results:Compared with the NG,the rabbit tear secretion decreased and the BUT was shortened in the MG(both P<0.01);compared with the MG and the SEAG,the rabbit tear secretion increased and the BUT was prolonged in the EAG(all P<0.05).Compared with the NG,the apoptosis of rabbit conjunctival cells increased(P<0.01),the expressions of Caspase-3 and Fas proteins increased(both P<0.05),and the expression of Bcl-2 protein decreased(P<0.01)in the MG;compared with the MG and the SEAG,the apoptosis of rabbit conjunctival cells decreased(both P<0.01),the expressions of Caspase-3 and Fas proteins decreased(all P<0.05),and the expression of Bcl-2 protein increased(both P<0.01)in the EAG.Conclusion:EA can inhibit the apoptosis of rabbit conjunctival cells,down-regulate the expressions of apoptosis-related proteins Caspase-3 and Fas,and up-regulate the expression of Bcl-2 protein,which may be one of the mechanisms of EA in treatment of DES.
文摘We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneal y for 12 weeks. Myocardial injury indices and oxidative stress markers were determined. Changes in cardiac ultrastructure were evaluated with transmission electron microscopy. Myocardial apoptosis was assessed via terminal deoxynucleotidyl transferase （TDT）-mediated DNA nick-end labeling （TUNEL） and immunohistochemistry. Ginsenoside Rg1 was as-sociated with a significant dose-dependent reduction in serum levels of creatinine kinase MB and cardiac troponin I, and lessened ultrastructural disorders in diabetic myocardium, relative to the untreated diabetic model rats. Also, compared with the untreated diabetic rats, significant reductions in serum and myocardial levels of malondialdehyde were noted in the ginsenoside Rg1-treated groups, and increased levels of the antioxidants （superoxide dismutase, catalase, and glutathione peroxidase） were detected. TUNEL staining indicated reduced myocardial apoptosis in ginsenoside Rg1-treated rats, which may be associated with reduced levels of caspase-3 （CASP3） and increased levels of B-cell lymphoma-extra-large （Bcl-xL） in the diabetic myocardium. Ginsenoside Rg1 treatment of diabetic rats was associated with reduced oxidative stress and attenuated myocardial apoptosis, suggesting that ginsenoside Rg1 may be of potential preventative and therapeutic value for cardiovascular injury in diabetic patients.
