敌百虫经ERK1/2通路影响类固醇激素的合成

Trichlorfon inhibits steroidogenesis expression via ERK1 /2 signal pathway

目的初步探讨细胞外信号调节激酶(ERK1/2)通路在敌百虫抑制小鼠睾丸间质细胞瘤细胞(MLTC-1)类固醇激素合成中的作用。方法运用放射免疫法检测不同浓度敌百虫及加入ERK1/2通路抑制剂UO126后对MLTC-1细胞孕酮合成的影响;采用蛋白质印迹技术(Western-blot)检测敌百虫对ERK1/2磷酸化表达的影响。结果敌百虫显著抑制MLTC-1细胞孕酮的合成,并且随敌百虫剂量的增加,孕酮合成量呈下降趋势;当同时加入UO126后,随敌百虫染毒剂量的升高孕酮合成量的下降趋势更为明显;敌百虫与UO126一样能明显抑制ERK1/2的磷酸化,而对总ERK1/2表达无明显影响。结论在本试验条件下,敌百虫能明显抑制MLTC-1细胞的孕酮合成,其机制可能是通过ERK1/2通路。

Objective To investigate the role of extracellular signal regulated kinase （ERK1/2） signal pathway in the inhibition of steroidogenesis of MLTC-1 cells by trichlorfon. Methods After treated with different concentrations of trichlorfon with or without UO126,the progesterone secretion of MLTC-1 cells was detected by RIA. Western blot analysis was used to assess the expression of ERK1 /2 phosphorylation. Results The progesterone production of MLTC-1 cells was decreased in a dose-effect manner depending on trichlorfon concentration; When UO126 was added to the medium,a more significant reduction was observed than without UO126; Trichlorfon,as same as UO126,inhibited ERK1 /2 phosphorylation but did not affect the total expression of ERK1 /2. Conclusion Trichlorfon can inhibit progesterone production through ERK1 /2 signal pathway in MLTC-1 cells.