葛根素对双酚S致睾酮合成损伤的保护作用
摘要
方法:用 25、50、100 mg/L BPS处理小鼠睾丸间质细胞(TM3)48 h并用 30 mg/L PUE进行干预,ELISA法检测睾
酮水平,试剂盒检测检测氧化应激指标 CAT、GSH、SOD、MDA和ROS的水平,Western blot检测细胞中 StAR和
MAPK信号通路相关蛋白表达水平。结果:BPS处理 48 h后,TM3细胞活性降低且呈剂量依赖性,同时睾酮水平降
低,经 PUE干预后睾酮水平增加。BPS引起细胞中 SOD、CAT和 GSH的活力降低,而ROS和MDA水平增加,而
PUE干预后抗氧化剂的活力增加,ROS和MDA水平降低。BPS暴露引起 StAR蛋白表达水平降低(P< 0.05),经过
PUE处理后 StAR水平增加。BPS处理后 p38/JNK MAPK信号通路上相关蛋白表达水平升高,磷酸化水平升高,PUE
干预后MAPK信号通路磷酸化水平降低。结论:BPS诱导TM3细胞发生氧化应激,激活 p38/JNK MAPK信号通路,
抑制睾酮合成,是BPS诱导雄性毒性的一种可能机制。PUE能减轻BPS引起的TM3细胞毒性作用。
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图4 BPS处理与PUE干预对TM3细胞p38/JNK MAPK信号通路的影响
(A和B)TM3细胞中 p38 MAPK细胞通路的蛋白表达水平;(C和D)TM3细胞中 JNK MAPK信号通路的蛋白
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