子宫内膜异位症模型大鼠接受米非司酮干预后炎性因子、侵袭和凋亡基因表达的评估

摘要

Objective: To study the effect of mifepristone intervention on the inflammatory factor as well as invasion and apoptosis gene expression in endometriosis lesions of endometriosis model rats.Method: SD female rats were selected as experimental animals, divided into model group (EMs group) and mifepristone group (RU486 group) and made into endometriosis models, then the EMs group received saline intervention and RU486 group received 2.6mg/kg/d RU486 intervention.4 weeks after intervention, endometriosis lesions were anatomized to determine the expression of inflammatory factors (COX-2, PGE2, TNF-α, IL-1β and IL-6), invasion genes (OPN, MMP2, MMP9, uPA and S100A6) as well as apoptosis genes (Bcl-2, Livin, Smac and PTEN).Results: COX-2, PGE2, TNF-α, IL-1β, IL-6, OPN, MMP2, MMP9, uPA, S100A6, Bcl-2 and Livin protein expression in endometriosis lesions of Ru486 group were significantly lower than those of EMs group while Smac and PTEN protein expression were higher than those of EMs group.Conclusion: Mifepristone for endometriosis model rats can inhibit the expression of inflammatory factors, invasion genes and anti-apoptosis genes, and increase the expression of pro-apoptosis genes.%目的:研究米非司酮干预对子宫内膜异位症模型大鼠子宫内膜异位病灶中炎性因子、侵袭和凋亡基因表达量的影响.方法:选择SD雌性大鼠作为实验动物并分为模型组(EMs组)和米非司酮组(RU486组),建立子宫内膜异位症模型后EMs组给予生理盐水干预、RU486组给予2.6 mg·kg-1·d-1 RU486干预.干预后4周,解剖子宫内膜异位病灶并测定炎性因子(COX-2、PGE2、TNF-α、IL-1β、IL-6)、侵袭基因(OPN、MMP2、MMP9、uPA、S100A6)、凋亡基因(Bcl-2、Livin、Smac、PTEN)的表达量.结果:Ru486组大鼠子宫内膜异位病灶中COX-2、PGE2、TNF-α、IL-1β、IL-6、OPN、MMP2、MMP9、uPA、S100A6、Bcl-2、Livin的蛋白表达量均显著低于EMs组,Smac、PTEN的蛋白表达量高于EMs组.结论:米非司酮用于子宫内膜异位症模型大鼠能够抑制炎性因子、侵袭基因、凋亡抑制基因的表达,增加促凋亡基因的表达.