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目的探讨全氟辛烷磺酸(PFOS)诱导人肝肿瘤Hep G_2细胞凋亡的机制。方法采用CCK-8试剂盒检测PFOS对Hep G_2细胞增殖的抑制作用;采用不同剂量PFOS染毒48 h后流式细胞术分析细胞凋亡率;JC-1试剂盒法检测线粒体膜电位;Hoechst 33258染色法观察凋亡细胞核的形态学改变;实时荧光定量PCR技术(Real-time-PCR)检测Cytochrome C、Caspase-3、AIF和Bax等凋亡相关蛋白mRNA表达水平。结果 PFOS对Hep G_2细胞增殖有明显的抑制作用;流式细胞术分析结果显示随着PFOS浓度的增加Hep G_2细胞凋亡率逐渐增加;PFOS染毒使线粒体膜电位降低并使细胞凋亡相关蛋白Cytochrome C、Caspase-3、AIF以及Bax的mRNA表达量增加。结论 PFOS可抑制Hep G_2细胞增殖并诱导其凋亡,其机制可能与影响Cytochrome C、Caspase-3、AIF和Bax等凋亡相关因子的mRNA表达水平有关。
Objective To investigate the mechanism of perfluorooctane sulfonate (PFOS) -induced apoptosis in human hepatocarcinoma Hep G 2 cells. Methods The inhibitory effect of PFOS on the proliferation of Hep G2 cells was detected by CCK-8 kit. The apoptotic rate was analyzed by flow cytometry 48 h after exposure to different doses of PFOS. The mitochondrial membrane potential was measured by JC-1 kit assay. Hoechst 33258 The morphological changes of apoptotic nuclei were observed by the staining method. The mRNA expression of apoptosis-related proteins such as Cytochrome C, Caspase-3, AIF and Bax were detected by real-time-PCR. Results PFOS significantly inhibited the proliferation of Hep G2 cells. Flow cytometry analysis showed that the apoptotic rate of Hep G2 cells increased gradually with the increase of PFOS concentration. PFOS exposure reduced the mitochondrial membrane potential and increased the expression of apoptosis related proteins Cytochrome C, Caspase-3, AIF and Bax mRNA expression increased. Conclusions PFOS can inhibit the proliferation and induce the apoptosis of Hep G2 cells. The mechanism may be related to the mRNA expression of apoptosis-related factors such as Cytochrome C, Caspase-3, AIF and Bax.