米非司酮治疗大鼠子宫内膜异位症发病TGFβ―Smad机制研究.docVIP

米非司酮治疗大鼠子宫内膜异位症发病TGFβ―Smad机制研究 　　[摘要] 目的 分析大鼠子宫内膜异位症发病的TGFβ-Smad信号通路参与机制及米非司酮的改善作用。 方法 将雌性SD大鼠随机分为假手术组、子宫内膜异位症模型组、小剂量和大剂量米非司酮组（n=10）。采用免疫印迹法检测各组大鼠异位组织中TGFβ-Smad信号通路的关键蛋白及细胞凋亡蛋白Bax、Bcl-2和Caspase-3的表达。结果 子宫内膜异位症模型组大鼠的TGFβ-Smad信号通路关键蛋白TGFβ、Smad1、Smad2及Smad3的表达均明显增高（P0.01）；促细胞凋亡蛋白Bax及Caspase-3表达增强而Bcl-2表达降低（P0.01）；米非司酮组大鼠的上述蛋白的异常得到显著恢复（P0.01或P0.05），且大剂量组效果明显优于小剂量组（P0.05）。 结论 米非司酮可通过抑制激活的TGFβ-Smad通路改善大鼠子宫内膜异位症的异常。 　　[关键词] 子宫内膜异位症；TGFβ-Smad信号通路；米非司酮；细胞凋亡 　　[中图分类号] R711.71 [文献标识码] A [文章编号] 1673-9701（2017）09-0039-04 　　Study on the effect of mifepristone on the TGFβ-Smad mechanism of the pathogenesis of endometriosis in rats 　　CHEN Xuwei GUO Jinfang LI Huaqing 　　Department of Gynecology， Dongyang People’s Hospital in Zhejiang Province， Dongyang 322100， China 　　[Abstract] Objective To analyze the mechanism of TGFβ-Smad signaling pathway in the pathogenesis of endometriosis in rats and the improvement of mifepristone. Methods Female SD rats were randomly divided into sham operation group， endometriosis model group and mifepristone low dose group and high dose group（n=10）. The expression of key proteins in the TGFβ-Smad signaling pathway and the expression of apoptosis proteins such as Bax， Bcl-2 and Caspase-3 in ectopic tissues of rats were detected by immunoblotting method. Results The expression of key proteins in the TGFβ-Smad signalling pathway such as TGFβ， Smad1， Smad2 and Smad3 were significantly increased in the rats in the endometriosis model group（P0.01）； the expression of apoptosis proteins such as Bax and Caspase-3 was increased and the expression of Bcl-2 was decreased（P0.01）； the abnormalities of the above proteins in the mifepristone group were significantly recovered（P0.01 or P0.05）， and the effect in the high dose group was significantly better than that in the low dose group（P0.05）. Conclusion Mifepristone can improve the abnormalities of endometriosis in rats by inhibiting the activated TGFβ-Smad pathway. 　　[Key words] Endometriosis； TGFβ-Smad signa