首页> 外文期刊>The Journal of toxicological sciences >Methylmercury induces CCL2 expression through activation of NF-κB in human 1321N1 astrocytes.
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Methylmercury induces CCL2 expression through activation of NF-κB in human 1321N1 astrocytes.

机译:甲基汞通过激活人类1321N1星形胶质细胞中的NF-κB诱导CCL2表达。

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摘要

Methylmercury is an environmental pollutant that is toxic to the central nervous system; however, the molecular mechanisms underlying its toxicity remain unclear. Methylmercury increases expression of several chemokines in the cerebellum of mice treated with methylmercury. The present study analyzes the mechanism underlying methylmercury-induced chemokine expression using human 1321N1 astrocytes, and shows that methylmercury increases CCL2 expression in these cells. The transcription factor NF-κB is involved in the induction of chemokine expression. Methylmercury increased the level of the NF-κB p65 subunit in the nuclei of 1321N1 cells. The methylmercury-induced increase in CCL2 expression was significantly decreased by suppression of p65 expression by RNA interference. These results suggest that methylmercury induces chemokine expression through activation of NF-κB in human astrocytes.
机译:甲基汞是对中枢神经系统有毒的环境污染物。然而,其毒性的分子机制仍不清楚。甲基汞增加了用甲基汞治疗的小鼠小脑中几种趋化因子的表达。本研究分析了使用人类1321N1星形胶质细胞诱导甲基汞诱导的趋化因子表达的机制,并表明甲基汞增加了这些细胞中CCL2的表达。转录因子NF-κB参与趋化因子表达的诱导。甲基汞增加了1321N1细胞核中NF-κBp65亚基的水平。甲基汞诱导的CCL2表达增加通过RNA干扰抑制p65表达而明显降低。这些结果表明甲基汞通过激活人星形胶质细胞中的NF-κB诱导趋化因子表达。

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