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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、200μmol/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、200μmol/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,200μmol/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。
Objective To investigate the apoptosis of N9 cells induced by perfluorooctane sulfonate (PFOS) via the mitochondria pathway using microglia cell line (N9) as a target cell. Methods 5,10,50,100,200 μmol / L PFOS exposure group and control group were set. 24 h after PFOS exposure, apoptotic cells were analyzed by flow cytometry. Mitochondrial membrane potential was detected by rhodamine 123. The apoptosis-related genes p53, Bax, Bcl-2, caspase-3 and caspase were detected by fluorescence quantitative PCR 24 h after exposure to PFOS. -9 expression. Results Compared with the control group (2.24%), the apoptotic rates in 50,100,200μmol / L PFOS group were significantly increased (20.81%, 33.26%, 48.72%, P <0.05) In addition, the expression of p53, Bax, caspase-3 and caspase-9 genes in PFOS-treated groups increased with the increase of dose, and the expression of Bcl-2 was increased Down trend, but no concentration dependence. Conclusion Exposure to PFOS can destroy the autogas at glial cells, destroy mitochondria, affect the expression of apoptosis-related genes and induce neuronal apoptosis.