全氟辛烷磺酸诱导HepG2细胞凋亡的线粒体损伤机制研究

doi:10.13217/j.scjpm.2016.0006

华南预防医学 ›› 2016, Vol. 42 ›› Issue (1): 6-10.doi: 10.13217/j.scjpm.2016.0006

全氟辛烷磺酸诱导HepG2细胞凋亡的线粒体损伤机制研究

马艳^1，2，李梦承³，李文学²，杨光宇²，殷花¹，章霞¹，李军涛²，吴锦银²，朱伟²，张波¹

1.中山大学公共卫生学院，广东广州 510080；2.广州市疾病预防控制中心；3.南方医科大学公共卫生与热带医学院

收稿日期:2015-12-07 出版日期:2016-02-20 发布日期:2016-05-16
通讯作者: 朱伟,张波 E-mail:zhuyc126@126.com；zhangb65@mail.sysu.edu.cn；
作者简介:马艳（1988—），女，在读硕士研究生，研究方向：生化与分子毒理学

Potential mechanism of mitochondrial damage in PFOS-induced HepG2cell apoptosis

MA Yan^1,2, LI Meng-cheng³, LI Wen-xue², YANG Guang-yu², YIN Hua¹, ZHANG Xia¹, LI Jun-tao², WU Jin-yin², ZHU Wei², ZHANG Bo¹

1. School of Public Health, Sun Yat-sen University, Guangzhou 510080, China; 2. Guangdong Provincial Center for Disease Control and Prevention; 3. Southern Medical University, School of Public Health and Tropical Medicine

Received:2015-12-07 Online:2016-02-20 Published:2016-05-16

摘要/Abstract

摘要： 目的探讨全氟辛烷磺酸（PFOS）诱导人肝肿瘤HepG2细胞凋亡的机制。方法采用CCK-8试剂盒检测PFOS对HepG2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HepG2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HepG2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HepG2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。

Abstract: ObjectiveTo explore effects of perfluorooctane sulphonate (PFOS) on proliferation and apoptosis of HepG2 cells and the potential mechanism of mitochondrial damage.MethodsA model based on human HepG2 cells exposed to various concentrations of PFOS for 48 hours was utilized to examine the effects of PFOS on cell proliferation and apoptosis. Cell proliferation was measured with CCK-8 cell counting kit. Mitochondrial membrane potential (MMP) was measured by using JC-1 assay kit. The morphological changes of the nucleus were observed with fluorescent inverted microscope after staining the cells with Hoechst 33258. Cell cycle distribution and apoptotic rate were evaluated with flow cytometry (FCM). Quantitative real-time RT-PCR was used to detect the mRNA expressions of apoptosis related factors including Cytochrome C, Caspase-3, AIF, and Bax. ResultsPFOS could inhibit the proliferation of HepG2 cells evidently. According to FCM analysis, the apoptotic rate of HepG2 cells increased with increasing the doses of PFOS. The dissipation of MMP was observed after exposure to PFOS. The mRNA expressions of Cytochrome C, Caspase-3, AIF, and Bax were up-regulated. ConclusionPFOS could inhibit the proliferation and induce apoptosis of HepG2 cells. The mechanism might be associated with changing of the mRNA expressions including Cytochrome C, Caspase 3, AIF, and Bax.

中图分类号:

R114

马艳，李梦承，李文学，杨光宇，殷花，章霞，李军涛，吴锦银，朱伟，张波. 全氟辛烷磺酸诱导HepG2细胞凋亡的线粒体损伤机制研究[J]. 华南预防医学, 2016, 42(1): 6-10.

MA Yan^1,2, LI Meng-cheng³, LI Wen-xue², YANG Guang-yu², YIN Hua¹, ZHANG Xia¹, LI Jun-tao², WU Jin-yin², ZHU Wei², ZHANG Bo¹. Potential mechanism of mitochondrial damage in PFOS-induced HepG2cell apoptosis[J]. S China J Prev Med, 2016, 42(1): 6-10.

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全氟辛烷磺酸诱导HepG2细胞凋亡的线粒体损伤机制研究

Potential mechanism of mitochondrial damage in PFOS-induced HepG2cell apoptosis

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