mTOR信号通路在镉诱导PC12细胞凋亡和Bcl-2、Bax蛋白表达中的作用

Effects of mTOR signaling pathway on apoptosis and the protein expression of Bcl-2,Bax in PC12 cells treated by cadmium

为研究雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号通路在镉诱导神经细胞凋亡和相关蛋白Bcl-2、Bax表达中的作用,用醋酸镉和/或雷帕霉素(rapamycin,Rap)染毒PC12细胞24h,流式细胞术检测细胞凋亡率,Hoechst33258荧光染色法检测细胞凋亡形态学变化,Western blot法检测Bcl-2和Bax蛋白表达水平。结果显示:与对照组相比,染毒组细胞凋亡和Bax蛋白表达水平升高,Bcl-2蛋白表达水平降低,Bcl-2/Bax极显著降低(P<0.01);与镉染毒组相比,镉与Rap联合作用组细胞凋亡和Bax蛋白表达水平降低,Bcl-2蛋白表达水平升高,Bcl-2/Bax显著升高(P<0.05)。结果表明:镉可能通过激活mTOR信号通路调节Bcl-2和Bax的表达,从而诱导神经细胞凋亡。

To investigate the effects of mTOR signaling pathway on apoptosis and expression of apoptosis-related proteins Bcl-2, Bax in neuronal cells, PC12 cells were exposured to cadmium and/or rapamycin （Rap） for 24 h. Then,the apoptosis rates were detected by flow cytometry,the morphological changes of apoptosis were observed by Hoechst33258 staining,and the protein lev- els of Bcl-2 and Bax were assayed by Western blot. In comparison with the control group, the re- sults showed that levels of apoptosis and Bax protein increased, Bcl-2 decreased, Bcl-2/Bax de- creased significantly（P^0.01）. Compared to the poisoning groups,levels of apoptosis and Bax protein decreased,Bcl-2 increased, Bcl-2/Bax increased significantly（P〈0.05） in the presence of cadmium and Rap groups. It was concluded that cadmium may regulate the expression of Bcl-2 and Bax by activating mTOR signaling pathway,resulting in neuronal apoptosis.