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，10，20 μmol·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；10，20 μmol·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 IV on the autophagy of cardiomyocytes induced by ischemia，and to explore the myocardial protection and mechanism of astragaloside IV. Methods The neonatal ischemia cardiomyocyte model was established. By using the methods of molecular biology and immunocytochemistry，the changes of cardiomyocyte autophagy and injury in ischemia model before and after being treated with astragaloside IV were observed. Results The process of cardiomyocyte autophagy could be activated by ischemia which will induce the death of cardiomyocyte. The astragaloside IV medicated serum could recover the cardiomyocyte injury induced by ischemia obviously. Astragaloside IV at 10 and 20 μmol·L-1 recovered the activity of cells to 80 %(P < 0.05) and 85 %(P < 0.05)，and decreased the number of apoptotic cells to 2.6(P < 0.05) and 1.8(P < 0.05) times of normal group，respectively. The above effects were dose-dependently. Furthermore，the astragaloside IV medicated serum could promote the expression of autophagy protein LC3 and inhibit the expression of Beclin 1 protein. Aastragaloside IV at 10 and 20 μmol·L-1 increased the level of autophagy protein LC3 to the 1.5(P < 0.05) and 1.7(P < 0.05) times of normal group. Conclusion Astragaloside IV can recover the cardionmyocytes activity which is decreased by ischemia，and decrease the myocardial cell apoptosis induced by ischemia. The mechanism may be related with promoting the autophagy of cardiomyocytes induced by ischemia.

广东省自然科学基金(8151040701000046)。