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目的:探讨黄芪甲苷(Astragaloside IV,ASIV)对异丙肾上腺素(Isoproterenol,ISO)诱导的H9C2心肌细胞凋亡的抑制作用及机制。方法:H9C2心肌细胞传代后随机分为正常对照组、异丙肾上腺素(10μmol/L)组、普萘洛尔(2μmol/L)组和黄芪甲苷(25、50、100μmol/L)组,采用流式细胞术检测H9C2心肌细胞凋亡率;运用JC-1荧光探针检测各组细胞线粒体膜电位的变化;采用Western Blot分别测定线粒体和胞浆中细胞色素C(Cytochrome C,Cyt-C)的蛋白表达。结果:与正常对照组相比,异丙肾上腺素组的凋亡率显著增加,线粒体膜电位降低,细胞色素C外流,线粒体细胞色素C表达减少而胞浆中表达增多。与模型组相比,黄芪甲苷(50、100μmol/L)组能明显降低凋亡率,提高线粒体膜电位及减少细胞色素C外流,且呈一定剂量依赖性。结论:黄芪甲苷可通过线粒体凋亡途径抑制异丙肾上腺素诱导的心肌细胞凋亡。
Objective: To investigate the inhibitory effect of Astragaloside IV (ASIV) on isoproterenol (ISO)-induced apoptosis of H9C2 cardiomyocytes and its mechanism. METHODS: H9C2 cardiomyocytes were randomly divided into normal control group, isoproterenol (10 μmol/L) group, propranolol (2 μmol/L) group and astragaloside (25, 50, 100 μmol/L) group. Flow cytometry was used to detect the apoptosis rate of H9C2 cardiomyocytes; JC-1 fluorescent probe was used to detect the changes of mitochondrial membrane potential in each group; Western Blot was used to determine cytochrome C in mitochondria and cytoplasm (Cytochrome C, Cyt-C). ) Protein expression. RESULTS: Compared with the normal control group, the apoptotic rate in the isoproterenol group was significantly increased, the mitochondrial membrane potential was decreased, cytochrome C flowed out, and the mitochondrial cytochrome C expression was decreased while the expression in the cytoplasm was increased. Compared with the model group, astragaloside (50, 100 μmol / L) group can significantly reduce the rate of apoptosis, increase mitochondrial membrane potential and reduce the cytochrome C outflow, and showed a dose-dependent manner. CONCLUSION: Astragaloside IV can inhibit isoprenaline-induced cardiomyocyte apoptosis through mitochondrial apoptosis pathway.