目的 研究黄芪总皂苷(ASTs)对H2O₂诱导心肌细胞凋亡的保护作用及相关调控蛋白Hsp-70、Caspase-3、Bcl-2、Bax表达的影响。方法(1)常规方法培养大鼠乳鼠心肌细胞，分为正常对照组、模型组及黄芪总皂苷4个剂量组(20，40，80，100 mg·L-1)，四甲基偶氮唑蓝(MTT)法观察黄芪总皂苷不同浓度对H2O₂损伤心肌细胞存活率的影响；(2)乳鼠心肌细胞培养后分为正常对照组、模型组、黄芪总皂苷(100 mg·L-1)预处理组，细胞免疫组化法和免疫印迹法(Western-blotting)分别检测Bcl-2、Bax、Hsp-70、Caspase-3的表达。结果(1)各黄芪总皂苷各组与模型组比较，细胞存活率明显增高，差异均有统计学意义(P < 0.05，P < 0.01)，且与黄芪总皂苷呈剂量依赖性；(2)与正常对照组比较，模型组Bcl-2、Hsp-70有少量表达，Bax、Caspase-3表达明显增多，黄芪总皂苷(100 mg·L-1)组与模型组比较，明显促进Bcl-2、Hsp-70的表达，降低Bax、Caspase-3的表达。结论黄芪总皂苷对心肌细胞具有良好的抗氧化保护作用，且呈剂量依赖性，其作用机制可能是通过上调Bcl-2、Hsp-70及下调Bax、Caspase-3的表达来实现。

Objective To investigate the protective effects of astragalosides(ASTs) on the apoptosis of myocardial cells induced by hydrogen peroxide(H2O₂) and on the expression of apoptosis-related proteins of Hsp-70，Caspase-3，Bcl-2，and Bax. Methods In the first experiment，neonatal rat myocardial cells were cultured with the conventional method，and then the cultured cells were divided into normal control group，model group and ASTs pretreatment groups at the concentrations of 20，40，80，100 mg·L-1. Methyl thiazolyl tetrazolium(MTT) method was adopted to observe ASTs at different concentrations on the survival rate of injured myocardial cells induced by H2O₂. In the second experiment，cultured neonatal rat myocardial cells were divided into the normal control group，model group，ASTs pretreatment group(100 mg·L-1)，immunocytochemistry and Western blotting were used to detect the expression of Bcl-2，Bax，Hsp-70，and Caspase-3. Results In experiment one，the cell survival rate of ASTs pretreatment groups was increased significantly compared to the model group(P < 0.05，P < 0.01)，and the cell survival rate was positively correlated with ASTs concentrations. In experiment two，model group had a small quantity of Bcl-2 and Hsp-70 expression，and had obvious expression of Bax and Caspase-3 compared to the normal control group. ASTs group increased the expression of Bcl-2 and Hsp-70，and decreased the expression of Bax and Caspase-3 significantly compared to the model group. Conclusion ASTs has good antioxidation on the myocardial cells with a dose-dependent manner，and its mechanism may be through the up-regulation of Bcl-2 and Hsp-70，and through the down-expression of Caspase-3 and Bax.

R285.5

国家自然科学基金资助项目(30973895)；广东省科技计划项目(20090315)。