GYY4137通过Bcl-2/Bax/Cleaved caspase-3信号通路改善柯萨奇病毒B_3引起的大鼠乳鼠心肌细胞凋亡  

GYY4137 Ameliorates Coxsackie Virus B_3-induced Apoptosis of Neonatal Rat Myocardial Cells via Bcl-2/Bax/Cleaved caspase-3 Signal Pathway

作　　者：吴祖波 彭华[1] 白燕[1] 林雯[1] 张志泉[1] 刘亚黎[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院儿科,武汉430022

出　　处：《华中科技大学学报（医学版）》2014年第4期371-375,共5页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：国家自然科学基金青年基金资助项目(No.81300098);中央高校基本科研业务费专项资助项目(No.01-18-530196)

摘　　要：目的探讨外源性H2S对柯萨奇病毒B3引起的大鼠乳鼠心肌细胞凋亡的影响及其作用机制。方法培养SD大鼠乳鼠原代心肌细胞,建立病毒性心肌炎(viral myocarditis,VMC)体外模型,随机分为正常组、模型组、模型组+50μmol/L GYY4137组、正常组+50μmol/L GYY4137组。Hoechst 33342染色法及流式细胞术分别检测心肌细胞凋亡,TBA法及酶标法分别检测各组细胞丙二醛(MDA)、超氧化物歧化酶(SOD)的表达,Western blot法检测各组细胞Bcl-2、Bax、Cleaved caspase-3蛋白的表达。结果与模型组比较,给予50μmol/L GYY4137后,心肌细胞凋亡明显好转(P<0.01);50μmol/L GYY4137能使模型组心肌细胞MDA显著降低、SOD明显增加(均P<0.05);给予50μmol/L GYY4137后,模型组心肌细胞Bcl-2蛋白表达增加、Bax蛋白表达明显降低(均P<0.05)、Cleaved caspase-3蛋白表达显著降低(P<0.05);单纯给予50μmol/L GYY4137对正常心肌细胞上述各项检测指标无明显影响(均P>0.05)。结论GYY4137可显著改善柯萨奇病毒B3引起的大鼠乳鼠心肌细胞凋亡,其作用机制与抑制Bcl-2/Bax/Cleaved caspase-3信号通路激活有关。Objective To investigate the effect of exogenous H2 S on coxsackie virus B3（CVB3）-induced apoptosis of neonatal rat myocardial cells and its action mechanism.Methods The primary SD neonatal rat myocardial cells were cultured and used for establishment of the in vitro model of viral myocarditis（VMC）.They were randomly divided into normal group,model group,model group＋50μmol/L GYY4137,normal group＋50μmol/L GYY4137.Hoechst 33342 staining and flow cytometry were used to detect myocardial apoptosis,the TBA method and enzyme linked immunosorbent assay to detect the levels of malondialdehyde（MDA）and superoxide dismutase（SOD）and Western blot to measure the expression of Bcl-2,Bax and Cleaved caspase-3proteins in cells in each group.Results Compared with the model group,treatment with 50μmol/L GYY4137 significantly improved the myocardial apoptosis（P〈0.01）,reduced the level of MDA（P〈0.05）,and increased the level of SOD in myocardial cells（P〈0.05）;it conspicuously increased the expression level of Bcl-2protein,decreased the expression levels of Bax and Cleaved caspase-3proteins（P〈0.05）.Moreover,50μmol/L GYY4137 had no effects on these indexes in normal cardiomyocytes（P〉0.05）.Conclusion GYY4137 can significantly ameliorate the CVB3-induced apoptosis of cardiomyocytes by inhibiting the activation of Bcl-2/Bax/Cleaved caspase-3signal pathway.

关 键 词：硫化氢 病毒性心肌炎 柯萨奇病毒B3型 心肌细胞 凋亡 

分 类 号：R542.2[医药卫生—心血管疾病]