Fas/FasL信号通路在镉致PC12细胞凋亡中的作用及NAC的保护效应

Role of Fas/FasL signaling pathway in apoptosis of PC12 cells induced by cadmium and protective effect of NAC

为研究Fas/Fas L信号通路在镉致PC12细胞凋亡中的作用及N-乙酰半胱氨酸（NAC）的保护效应,本试验用10 mol/L醋酸镉和10 mg/L anti-Fas L抗体、40 mol/L Z-IETD-FMK、100 mol/L NAC单独或联合处理PC12细胞24 h后,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Fas、Fas L、FADD和cleaved caspase-8的蛋白表达量。结果,anti-Fas L抗体和Z-IETD-FMK极显著抑制镉致PC12细胞凋亡率升高（P〈0.01）;NAC极显著抑制镉致PC12细胞凋亡形态学变化,Fas、Fas L、FADD和Cleaved caspase-8蛋白表达量的升高（P〈0.01）。上述结果说明,镉可通过Fas/Fas L信号通路诱导PC12细胞凋亡,NAC在镉致PC12细胞凋亡Fas/Fas L信号通路中具有保护作用。

To investigate the role of Fas/Fas L signaling pathway in apoptosis of PC12 cells induced by cadmium（Cd）and protective effect of N-acetylcysteine（NAC）,PC12 cells were exposed to Cd（10 mol/L）and/or 10 mg/L anti-Fas L antibody,40 mol/L Z-IETD-FMK,100 mol/L NAC for 24 h.Then,cell apoptosis rates were measured by flow cytometry,morphological changes of apoptosis were observed by Hoechst33258 staining,protein levels of Fas,Fas L,FADD and cleaved caspase-8 were measured by Western-blot.The results showed that Cd-induced increase of apoptosis rates were inhibited by anti-Fas L antibody and Z-IETD-FMK significantly（P〈0.01）,morphological changes of apoptosis,as well as increased protein levels of Fas,Fas L,FADD and cleaved capase-8 were inhibited by NAC significantly（P〈0.01）.These findings suggest that Cd can induce apoptosis by Fas/Fas L signaling pathway in PC12 cells and NAC can provide protection against Cd-induced Fas/Fas L signaling pathway in PC12 cells.