中文摘要：

目的观察黄芪总苷（AST）在缺氧／复氧所致海马神经元凋亡的影响，探讨其抗损伤的作用机制。方法原代培养海马神经元细胞，建立缺氧／复氧损伤的海马神经元凋亡模型。采用DNA琼脂糖电泳和流式细胞术检测细胞凋亡；激光共聚焦显微镜检测细胞内游离钙离子浓度；Western blot法检测ERK和磷酸化ERK蛋白的表达。结果海马神经元细胞经缺氧／复氧后发生了明显凋亡形态学的改变，凋亡率增加，AST（20、40mg／L）能明显降低模型大鼠海马神经元凋亡百分率和胞质钙离子浓度，且促进磷酸化ERK蛋白水平的表达。结论黄芪总苷对脑缺血／再灌注所致损伤有一定的保护作用，其机制可能与抑制细胞钙超载、激活细胞ERK信号存活通路有关。

英文摘要：

Objective To study the effect of astragalosides （AST） on the injury induced by hypoxia/reoxygenation in primary cultures of rat hippocampal neurons. Methods Rat hippocampal neurons in primary culture were used, and a apoptosis model was induced by hypoxia/reoxygenation. The apoptosis rate of hippocampal neurons was analyzed by DNA ladder, flow cytometry with AnnexinV-FITC and PI staining. Intracellular free Ca^2＋ was observed with a co-focal laser microscope using fluo-3 acetoxymethylester as a fluorescent dye. Western blot was used to detect the protein expression of ERK, p-ERK. Results Compared to control group, AST（20,40 mg/L）could reduce the apoptosis rate and the damage degree of rat hippocampal neurons, and it could increase the expressing of p- ERK as well. Conclusion AST is protective effects on damaged neurons,the mechanism may be related to activating the ERK signaling transduction pathway.