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

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.