人参皂苷Rg1可能通过CDK4-pRB-E2F1通路减少神经元凋亡

目的　探讨人参皂苷Rg1是否通过CDK4 pRB E2F1通路对抗Aβ1～ 4 0 诱导的神经元凋亡。方法　用TUNEL染色、DNA琼脂糖凝胶电泳方法观察神经元凋亡形态学和生化改变 ;免疫印迹方法检测细胞周期相关的周期依赖性激酶4(Cyclindependentkinase 4,CDK4)、磷酸化的视网膜神经胶质瘤蛋白 (Retinoblastomaprotein ,pRB)水平 ;RT PCR技术检测E2F1mRNA表达水平 ;荧光分光光度计法检测凋亡效应分子Caspase 3活力的变化。结果　人参皂苷Rg1预处理可降低Aβ1～ 4 0 诱导的大鼠皮层神经元的凋亡率 ;凋亡细胞特有的DNA梯形条带消失 ;CDK4、磷酸化pRB水平降低 ;E2F1基因表达下调 ;Caspase 3活力下降。结论　人参皂苷Rg1可通过抑制CDK4 pRB E2F1信号传导通路及Caspase 3的激活 ,减少Aβ1～ 4 0 诱导的大鼠皮层神经元凋亡。

Ginsenoside Rg1 might attenuate apoptosis of neurons through CDK4-pRB-E2F1 pathway

AIM To study whether ginsenoside Rg1 could inhibit Aβ 1～40 induced apoptosis in rat cortical neurons through CDK4 pRB E2F1 pathway. METHODS The TUNEL staining and gel electrophoresis were used to observe the morphological and biochemical changes of neurons' apoptosis; the levels of CDK4 and phosphorylated pRB were detected by immunoblotting; RT PCR was used to examine the mRNA expression of E2F1 while fluorescent spectrofluorometer was used to measure caspase 3 activity. RESULTS Ginsenoside Rg1 pre treatment could remarkably decreased the apoptotic ratio in cortical neurons induced by Aβ 1～40 ; DNA ladder was extinct; the levels of CDK4 and phosphorylated pRB were reduced; expression of E2F1 mRNA was downregulated and caspase 3 activity was decreased. CONCLUSION Ginsenoside Rg1 could attenuate apoptosis of rat cortical neurons by inhibiting CDK4 pRB E2F1 signal transductive pathway and inhibiting the activation of caspase 3.