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目的探讨诺美孕酮促进实验性大鼠子宫内膜异位症模型细胞凋亡及其作用机制。方法外科手术法建立大鼠子宫内膜异位症模型;HE染色观察异位内膜病理组织学改变;ELISA测定血清中抗子宫内膜抗体(EMAb)水平;West-ern blot检测异位内膜组织中Bcl-2、Bax、Caspase-9、Caspase-3蛋白的表达情况。结果诺美孕酮(0.5、1.5、15 mg.kg-1)异位内膜萎缩,间质疏松,腺体数目明显减少,腺腔萎缩;诺美孕酮呈剂量依赖性地降低异位内膜厚度和EMAb的浓度;诺美孕酮(0.5、1.5、15 mg.kg-1)异位内膜组织中Bax、Caspase-9和Caspase-3蛋白表达升高、Bcl-2蛋白表达降低。结论诺美孕酮(0.5、1.5、15 mg.kg-1)可促进大鼠子宫异位内膜细胞凋亡,其作用机制可能与降低EMAb水平、上调Bax和下调Bcl-2蛋白表达、激活细胞凋亡的内源性途径启动因子Caspase-9蛋白、激活执行因子Caspase-3蛋白表达有关。
Objective To investigate the effects of nomethesone on apoptosis in experimental rat endometriosis model and its mechanism. Methods The rat model of endometriosis was established by surgery. The pathological changes of ectopic endometrium were observed by HE staining. The levels of anti-endometrial antibody (EMAb) in serum were measured by ELISA. The expression of Bcl-2, Bax, Caspase-9 and Caspase-3 in tissues was detected. Results Nomegelide (0.5, 1.5, 15 mg.kg-1) ectopic endometrium atrophy, interstitial loose, the number of glands decreased significantly, glandular atrophy; nomegestrin in a dose-dependent manner to reduce the ectopic Membrane thickness and the concentration of EMAb. The expression of Bax, Caspase-9 and Caspase-3 in ectopic endometrium of nomegestrol (0.5,1.5,15 mg.kg-1) increased and the expression of Bcl-2 protein decreased. Conclusions Nomegestone (0.5, 1.5 and 15 mg.kg-1) can promote the apoptosis of ectopic endometrial cells in rats, which may be related to the decrease of EMAb level, up-regulation of Bax and down-regulation of Bcl-2 protein expression and activation The endogenous pathway of apoptosis is related to the activation of caspase-9 protein and the activation of caspase-3 protein.