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目的观察黄芪甲苷(AS)对缺血模型诱导的乳鼠心肌细胞自噬的影响,探讨黄芪甲苷的心肌保护作用及机制。方法建立乳鼠心肌缺血的细胞损伤模型,采用分子生物学及免疫细胞化学法观察心肌细胞在缺血模型及黄芪甲苷处理后的自噬与细胞损伤变化。结果心肌细胞的自体吞噬程序会被缺血刺激激活,缺血可致心肌细胞死亡。黄芪甲苷可明显恢复缺血处理诱导的心肌细胞损伤,10,20μmol·L-1的黄芪甲苷分别使细胞活性恢复至80%及85%(均P<0.05),使凋亡细胞数目降低至正常对照组的2.6倍及1.8倍(均P<0.05),且呈现出剂量依赖效应。同时,黄芪甲苷可促进自噬蛋白(LC3)的表达;10,20μmol·L-1的黄芪甲苷分别使细胞LC3升高至正常对照组的1.5倍及1.7倍(均P<0.05)。结论黄芪甲苷可恢复缺血降低的心肌细胞活性,降低缺血诱导的心肌细胞凋亡,其机制可能与促进缺血诱导的心肌细胞自噬相关。
Objective To observe the effect of astragaloside (AS) on autophagy in neonatal rat cardiomyocytes induced by ischemia and to explore the protective effect and mechanism of Astragaloside IV on myocardial cells. Methods The model of myocardial injury induced by myocardial ischemia in neonatal rats was established. The changes of autophagy and cellular damage in myocardial cells after ischemia and Astragaloside treatment were observed by molecular biology and immunocytochemistry. Results Cardiomyocytes autophagy process will be activated by ischemic stimulation, ischemia can cause myocardial cell death. Astragaloside could obviously restore the injury of cardiomyocytes induced by ischemia. Astragaloside at 10μmol·L -1 and 10μmol·L -1 respectively restored the cell activity to 80% and 85% (both P <0.05), and decreased the number of apoptotic cells 2.6 times and 1.8 times that of the normal control group (all P <0.05), and showed a dose-dependent effect. At the same time, astragaloside could promote the expression of autophagy protein (LC3). The cells treated with 10 and 20μmol·L-1 of Astragaloside IV increased the cell number of LC3 to 1.5 and 1.7 times of the normal control (all P <0.05). Conclusion Astragaloside can restore the activity of myocardial cells with decreased myocardial ischemia and decrease the apoptosis of myocardial cells induced by ischemia, which may be related to the promotion of ischemia-induced autophagy in cardiomyocytes.