诺美孕酮促进大鼠子宫内膜异位症细胞凋亡及其作用机制

Effect of nomegestrol acetate on the apoptosis of endometriosis in rat models and its mechanism

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。

Aim To explore the effect of nomegestrol acetate（NOMAc） on the apoptosis of endometriosis（EMs） in rat models and its mechanism.Methods The rat models of NOMAc were established by surgical operation method;histopathologic changes of ectopic endometrium were tested by HE staining;the level of antiendometrium antibody（EMAb） was tested by Elisa;the expression levels of apoptosis factors were tested by Western blot.Results NOMAc（0.5,1.5,15 mg·kg-1）shriveled ectopic endometrium;the number of endometrial gland was fewer;glandular cavity was smaller in NOMAc groups than those of model groups.NOMAc reduced dose-dependently the endometrial thickness and the level of EMAb.NOMAc（0.5,1.5,15 mg·kg-1）increased Caspase-9,Caspase-3 and Bax protein expression and reduced Bcl-2 protein expression.Conclusion The inhibitory effect of NOMAc on ectopic endometrium of rat models may be related to reducing the level of EMAb,increasing Bax,reducing Bcl-2 protein expression,and activating Caspase-9 and Caspase-3 protein expression in endogenous apoptosis pathway.