EGb761通过改善线粒体功能抑制无血清SH-SY5Y细胞的凋亡  

EGb761 inhibits serum deprivation-induced apoptosis of SH-SY5Y cell via improvement of mitochondrial function

作　　者：艾卫敏[1] 左剑斌[2] 邓小华[1] 赵修斌[2] 石纯[3] 

机构地区：[1]中南大学湘雅医学院基础学院,湖南长沙410013 [2]湘潭职业技术学院,湖南湘潭411102 [3]广州医学院人体解剖学教研室,广东广州510182

出　　处：《解剖学研究》2011年第5期331-334,共4页Anatomy Research

摘　　要：目的标准化银杏叶提取物EGb761被认为有神经保护作用,但作用机制不明。本研究旨在检测EGb761对无血清人类神经母细胞瘤SH-SY5Y型细胞的生长和凋亡的作用,以了解其神经保护机制。方法本研究通过检测线粒膜电位、细胞色素C氧化酶和线粒体ATP合成率来评估线粒体机能;通过检测细胞周期来了解细胞的生长状态。结果我们发现,EGb761使血清剥夺诱导细胞的细胞周期停留在G0/G1期而减弱其凋亡,这有可能是通过改善线粒体的功能而实现的。结论 EGb761通过调节线粒体机能促进营养因子非依赖的神经元存活。这些结果可能为EGb761的神经保护作用增添一个新的视角。Objective EGb761 has long been showed to have neuroprotective effects,but the neuroprotective mechanisms are unclear.In this study,we tested the effect of EGb761 on serum deprivation-induced apoptosis and inhibition of growth of SH-SY5Y cells.Methods This study tested mitochondrial function via measurement of mitochondrial membrane potential,cytochrome C oxidase and mitochondrial ATP synthesis,and test cell growth via measurement of cell cycle.Results We found that EGb761 treatment attenuated serum deprivation-induced cell apoptosis via induction of cell cycle arrest at G0/G1,which might be associated with maintenance of mitochondrial function.Conclusion These data suggested that EGb761 promote trophic factor-independent neuronal survival via maintenance of mitochondrial function.

关 键 词：EGB761 血清剥夺 细胞周期 线粒体功能 

分 类 号：R285.5[医药卫生—中药学]