大鼠子宫内膜异位症的细胞外信号调节激酶信号通路参与机制及来曲唑的改善作用  

The involvement of activated ERK signaling pathway in the pathogenesis of endometriosis and ameliorative effect of letrozol

作　　者：刘海彬[1] 

机构地区：[1]菏泽市立医院妇产科,山东菏泽274000

出　　处：《中国计划生育和妇产科》2015年第8期31-35,共5页Chinese Journal of Family Planning & Gynecotokology

摘　　要：目的分析大鼠子宫内膜异位症(endometriosis,EMs)的细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)信号通路参与机制及来曲唑的改善作用。方法将40只雌性SD大鼠随机分为4组,每组10只,即假手术(Sham)组、子宫内膜异位症模型(EMs)组、PD98059(PD)组及来曲唑(LE)组。自体移植法手术建立EMs模型,PD98059组及来曲唑组进行对应灌胃治疗。采用Western Blotting分析各组大鼠异位组织中ERK信号通路的关键蛋白甲基乙基酮(Methyl Ethyl Ketone,MEK)、细胞外信号调节激酶1/2(extracellular signal-regulated kinase,ERK1/2)、p MEK(extracellular regulated protein kinase)及p ERK1/2蛋白的表达及参与细胞外基质重构的基质金属蛋白酶2(matrix metalloproteinase,MMP2)及细胞凋亡蛋白Caspase3的表达。结果 EMs模型大鼠的ERK信号通路关键蛋白MEK、p MEK、ERK1/2及p ERK1/2的表达均增高(分别为123.6%、136.4%、144.7%、141.2%);MMP2及Caspase3的表达增强(分别为187.6%、134.7%);来曲唑组大鼠的上述蛋白的异常表达得到显著恢复,且较子宫内膜异位症模型组降低(P<0.05)。结论激活的ERK信号通路及其所诱导的细胞外基质重构和细胞凋亡参与了大鼠EMs的发生过程,来曲唑通过抑制激活的ERK通路改善EMs的异常。Objective To investigate the involvement of activated extracellular signal - regulated kinase （ERK） signaling transduction pathway in the pathogenesis of endometriosis （ EMs ） and the ameliorative effect of letrozol. Methods A total of 40 female SD rats were randomly divided into 4 groups ： sham group, EMs group, PD98059 group and letrozol group, with 10 rates in each group. The EMs models were duplicated by autop｜astic transplantation, PD98059 and letrozol group were garaged with corresponding drugs. The expression of ERK pathway related proteins Methyl Ethyl Ketone （ MEK）, extracellular signal - regulated kinase （ ERKI/ 2）, extracellular regulated protein kinase （pMEK）, pERK1/2 and matrix metalloproteinase （MMP2） as well as Caspase3 were detected by Western Blotting. Results The research showed that the expression of MEK, pMEK, ERK1/2, pERK1/2 were up -regulated greatly （ 123.6 % , 136.4 %, 144. 7 %, 141.2 % , 134. 7 % and 187. 6 % respectively）, the expression of MMP2 and Caspase3 were inceased （187.6 % ,134. 7 % respectively）. While those abnormal protein expressions of letrozol group normalized significantly, which were lower than those of EMs group （ P 〈 0. 05 ）. Conclusion Over - activated ERK signaling pathway and extracellular matrix recombination combined apoptosis are involved in the pathogenesis of EMs and ameliorative effect of letrozol mainly through normalizing the aforementioned parameters.

关 键 词：子宫内膜异位症 ERK信号通路 细胞外基质重构 细胞凋亡 

分 类 号：R711.71[医药卫生—妇产科学]