论文部分内容阅读
目的探索十溴联苯醚(PBDE-209)诱导小鼠海马神经元细胞凋亡的潜在机制。方法原代海马神经元细胞和海马神经元细胞系HT-22用0、6.25、12.5、25、50和100μg/mL PBDE-209处理24 h。检测原代海马神经元细胞SOD活性,MDA、NO和GSH的含量,用Annexin V/PI双染法检测海马神经元细胞系HT-22细胞凋亡情况,用免疫蛋白印迹Western blot检测Bax、Bcl-2、CHOP、GRP78、PERK和Caspase-12蛋白表达水平。结果染毒组原代海马神经元细胞和HT-22细胞系细胞存活率显著降低(P<0.05)。原代海马神经元细胞MDA、NO含量显著升高(P<0.05),GSH含量、SOD活性显著降低(P<0.05);原代海马神经元细胞的Bax/Bcl-2比值、CHOP、Caspase-12蛋白表达水平升高(P<0.05)。HT-22细胞系GRP78、PERK、Caspase-12表达水平和细胞凋亡率升高(P<0.05)。结论氧化应激和内质网应激可能参与PBDE-209诱导的海马神经元细胞凋亡过程。
OBJECTIVE: To investigate the potential mechanism of PBDE-209 in inducing neuronal apoptosis in hippocampus of mice. Methods Primary hippocampal neurons and hippocampal neuronal cell line HT-22 were treated with 0, 6.25, 12.5, 25, 50 and 100 μg / mL PBDE-209 for 24 h. The activities of SOD, MDA, NO and GSH in primary hippocampal neurons were detected. The apoptosis of hippocampal neuronal cell line HT-22 was detected by Annexin V / PI double staining. The expression of Bcl-2, Bcl- -2, CHOP, GRP78, PERK and Caspase-12 protein expression levels. Results The cell viability of primary hippocampal neurons and HT-22 cell lines was significantly decreased (P <0.05). The contents of MDA and NO in primary cultured hippocampal neurons increased significantly (P <0.05), and the contents of GSH and SOD decreased significantly (P <0.05). The ratio of Bax to Bcl-2, CHOP and Caspase- 12 protein expression increased (P <0.05). The expression of GRP78, PERK, Caspase-12 in HT-22 cell line and the apoptosis rate were increased (P <0.05). Conclusion Oxidative stress and endoplasmic reticulum stress may be involved in the apoptosis of hippocampal neurons induced by PBDE-209.