文档介绍：银杏叶提取物对6-OHDA诱导PC12细胞Bax和Bcl-2表达的影响
【摘要】目的探讨银杏叶提取物(Ginkgo biloba extract,GBE)对6-羟基多巴胺(6-hydroxydopamine,6-OHDA)诱导的PC12细胞凋亡的保护作用及其机制。方法经不同浓度GBE预处理体外培养的PC12细胞加入6-OHDA诱导多巴胺能神经元损伤模型,用4-甲基偶氮唑蓝(MTT)检测 PC12 细胞活力;流式细胞仪(FCM)测定PC12细胞凋亡百分比;采用免疫印迹法检测Bcl-2和Bax的表达水平。结果 100 μmol/L的6-OHDA处理PC12细胞24 h,细胞活力较正常对照组明显降低(P<);与模型组比较,GBE 20,40 μg/ml可明显减轻6-OHDA对PC12细胞的毒性,GBE可使细胞活性增强,降低凋亡百分比。与正常对照组比较,模型组Bax表达升高,而Bcl-2表达降低(P<)。与模型组比较,GBE各剂量组Bax降低,而Bcl-2升高,且呈剂量依赖性(P<)。结论 GBE对6-OHDA诱导的PC12细胞凋亡具有抑制作用,上调Bcl-2和下调Bax表达可能是其作用的机制之一。
【关键词】银杏叶提取物;PC12细胞;6-羟基多巴胺;细胞凋亡
Abstract: Objective To investigate the protective effect and the causal mechanism of Ginkgo biloba extract (GBE) against PC12 cellular apoptosis induced by 6-hydroxydopamine (6-OHDA). Methods Dopaminergic neuronal injury model was induced by addition of 6-OHDA into PC12 cells cultured in vitro and pretreated at different concentrations of GBE. Cell viability, apoptotic percentage, and the expression of Bax and Bcl-2 were assayed by MTT, FCM and immunoblotting, respectively. Results The livability of PC12 cells treated with 100 μmol/L 6-OHDA for 24 h was lower than that of the control group (P<). Compared with the 6-OHDA group, GBE at concentrations of 20 and 40 μg/ml could markedly rel
ieve the toxicity of 6-OHDA on PC12 cells, which suggested that GBE could increase the cellular activity and decrease the percentage of cellular apoptosis. The Bax expression was up-regulated in 6-OHDA groups and Bcl-2 expression was down-regulated (P<), compared with the control group. Compared with the 6-OHDA group, the Bax expression was down-regulated and Bcl-2 expression was up-regulated in GBE groups, in a dose-dependent manner (P<). The difference had statistic significance. Conclusions As one of the causal mechanisms, GBE has inhibitory effects on the apoptosis of the 6-OHDA-induced PC12 cells by up-regulating Bcl-2 expression and down-regulating Bax expression.
Key words: Ginkgo biloba extract;