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-OH-DA)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100μmol/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<0.01);与模型组比较,GBE 20,40μg/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<0.05)。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<0.05)。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。
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 con- centrations 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 ceils treated with 100 μmol/L 6 - OHDA for 24 h was lower than that of the control group （ P 〈 0.01 ）. Compared with the 6 - OHDA group, GBE at concentrations of 20 and 40 μg/ml could markedly relieve 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 - OH- DA groups and Bcl - 2 expression was down - regulated （ P 〈 0.05 ）, 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 〈 0.05 ）. 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.
出处
《徐州医学院学报》
CAS
2009年第4期218-221,共4页
Acta Academiae Medicinae Xuzhou
基金
江苏省脑病生物信息重点实验室开放课题（Jsb10702）
