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作 者:朱芬芳[1] 尹艳艳[1] 李卫平[1] 李维祖[1] 吴国翠[1] 公惠玲[1] 张文[1]
机构地区:[1]安徽医科大学药理学教研室,安徽合肥230032
出 处:《中国药理学通报》2009年第2期213-216,共4页Chinese Pharmacological Bulletin
基 金:安徽省人才开发基金资助项目(No2007Z0301);安徽省自然科学基金资助项目(No00144414);安徽省教育厅自然科学基金资助(NoKJ2008B301);安徽省高等学校青年教师科研资助项目(No2008jq1059zd);安徽省十五新药攻关项目(No01803016)
摘 要:目的探讨黄芪提取物在缺氧/复氧所致神经元损伤中的保护作用。方法原代培养大鼠海马神经元细胞,建立缺氧/复氧损伤的海马神经元凋亡模型。采用四唑盐(MTT)法和LDH释放法检测细胞活力;Hoechst染色、Annexin V/PI双染流式细胞术检测细胞凋亡;Western blot法检测AKT和磷酸化AKT蛋白的表达。结果经缺氧/复氧后细胞活力明显下降,出现凋亡典型的形态学特征,磷酸化AKT蛋白表达下降;黄芪提取物能明显提高损伤海马神经元细胞活力,降低细胞凋亡率,促进磷酸化AKT蛋白的表达。结论黄芪提取物对缺氧/复氧神经元具有保护作用,其机制可能与激活PI3K/AKT细胞信号通路有关。Aim To study the effect of EA 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. MTF assay and LDH releasing rate were used to detect the cell viability. The apoptosis rate of hipp-ocampal neurons was analyzed by Hoechst 33255 staining, flow cytometry with AnnexinV-FITC and PI staining. Western blot was used to detect the protein expression of AKT and p-AKT. Results Compared tocontrol group, three hours of hvnoxia followed by sixteen hours of reoxygenation induced hippocampal neuronal apoptosis. EA could raise the neuronal viability and reduce apoptosis rate and the damage degree of rat hippocampal neurons. EA could increase the expressing of p-AKT. Conclusions EA has protective effects on damaged neurons, and the mechanism may be related to activating the PI3K-AKT signal transduction pathway.
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