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张玲, 江中发, 张本延. 全氟辛烷磺酸盐通过线粒体途径诱导N9细胞凋亡[J]. 中国公共卫生, 2013, 29(2): 239-241. DOI: 10.11847/zgggws2013-29-02-27
引用本文: 张玲, 江中发, 张本延. 全氟辛烷磺酸盐通过线粒体途径诱导N9细胞凋亡[J]. 中国公共卫生, 2013, 29(2): 239-241. DOI: 10.11847/zgggws2013-29-02-27
ZHANG Ling, JIANG Zhong-fa, ZHANG Ben-yan. Mechanism of apoptosis and its pathway induced by perfluorooctane sulfonate(PFOS) in murine glial cells[J]. Chinese Journal of Public Health, 2013, 29(2): 239-241. DOI: 10.11847/zgggws2013-29-02-27
Citation: ZHANG Ling, JIANG Zhong-fa, ZHANG Ben-yan. Mechanism of apoptosis and its pathway induced by perfluorooctane sulfonate(PFOS) in murine glial cells[J]. Chinese Journal of Public Health, 2013, 29(2): 239-241. DOI: 10.11847/zgggws2013-29-02-27

全氟辛烷磺酸盐通过线粒体途径诱导N9细胞凋亡

Mechanism of apoptosis and its pathway induced by perfluorooctane sulfonate(PFOS) in murine glial cells

  • 摘要: 目的 以小胶质细胞株(N9)作为靶细胞,观察全氟辛烷磺酸盐(PFOS)通过线粒体途径诱发N9细胞凋亡效应。方法 设定5、10、50、100、200 μmol/L PFOS染毒组及对照组。PFOS染毒24 h后流式细胞术分析凋亡细胞率,罗丹明123检测线粒体膜电位,荧光定量PCR检测染毒24 h后凋亡相关基因p53、Bax、Bcl-2、caspase-3和caspase-9表达。结果 与对照组(2.24%)比较,50、100、200 μmol/L PFOS组细胞凋亡率(分别为20.81%、33.26%、48.72%)均增加(P<0.05);PFOS染毒降低了线粒体膜电位,200 μmol/L组细胞出现明显核周小斑点状荧光;此外,随剂量增加,PFOS染毒组p53、Bax、caspase-3和caspase-9基因表达水平呈上升趋势,Bcl-2表达水平呈下降趋势,但未见浓度依赖性。结论 PFOS暴露可破坏神经小胶质细胞自稳态,破坏线粒体,影响凋亡相关基因表达,诱导神经细胞凋亡。

     

    Abstract: Objective To evaluate the apoptosis of murine microghia N9 cells related to mitochondrial function after PFOS exposure.Methods The N9 cells were exposed to PFOS at concentrations 5,10,50,100,and 200 μmol/L for 24 and 48 hours,respectively,and the controls were exposed to 0.5% dimethyl sulfoxide(DMSO).The apoptotic celluar ratio was detected by flow cytometry 24 hours after the exposure.Mitochondrial membrane potential(MMP) was measured by Rhodamine 123 and the expressions of p53,Bax,Bcl-2,caspase-3,and caspase-9 mRNA were detected by real-time (RT)-PCR after the exposure for 24 and 48 hours.β-actin was used as the internal reference gene.Results Compared with the apoptotic ratio(2.24%) of the control group,statistically significant increases in apoptotic celluar ratio were observed in 50,100,and 200 μmol/L PFOS exposure groups(20.81%,33.26%,and 48.72%).The dissipation of MMP was observed with punctate perinuclear fluorescence after 200 μmol/L PFOS exposure.But no dose-dependent up-regulation of p53,Bax,caspase-3,and caspase-9 mRNAs,and down-regulation of Bcl-2 mRNA were involved after PFOS exposure.Conclusion The results suggest that cell apoptosis induced by PFOS is mainly mediated by mitochrondrial pathway,in which PFOS could disturb homeostasis of microglial cells,impact mitochondria,and affect gene expression of apoptotic regulators.

     

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