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作 者:朱芬芳[1] 李卫平[1] 尹艳艳[1] 李维祖[1]
出 处:《安徽医科大学学报》2009年第4期471-475,共5页Acta Universitatis Medicinalis Anhui
基 金:安徽省人才开发基金资助项目(编号:2007z030);安徽省自然科学基金资助项目(编号:00144414);安徽省教育厅基金资助项目(编号:KJ2009A81)
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;Westernblot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。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.
关 键 词:黄芪 植物提取物/药理学 细胞凋亡 海马 细胞外信号调节MAP激酶类
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