生存素基因在子宫内膜异位症中的表达及促性腺激素释放激素激动剂、环氧合酶-2抑制剂对其表达的影响

Survivin expression in endometriosis and normal human endometrium and effects of GnRH-a and COX-2 inhibitor on its expression.

目的探讨生存素（survivin）基因在子宫内膜异位症（FMs）发病机制中的作用。方法检测生存素在正常与异位子宫内膜组织中的表达；观察促性腺激素释放激素激动剂（GnRHa）、环氧合酶-2（COX-2）抑制剂对体外培养的EMs异位内膜细胞及正常子宫内膜细胞中survivin基因mRNA表达的调节作用及对体外培养的异位内膜凋亡率的影响。结果①EMs异位组、在位组survivin mRNA的表达明显强于对照组（均P〈0．05），且无周期性变化。②GnRHa可呈浓度依赖性下调体外培养的异位内膜细胞及正常子宫内膜细胞中survivin mRNA的表达，COX-2抑制剂亦呈浓度依赖性下调体外培养的异位内膜细胞及正常子宫内膜细胞中survivin mRNA的表达，GnRHa100μg／L加COX-2抑制剂40μmol／L可以促进体外培养的异位内膜细胞凋亡（P〈0．05），二者无明显协同作用（P〉0．05）结论①异位内膜细胞高表达survivin，对凋亡的敏感性低，使异位灶存活并发展；②GnRHa、COX-2抑制荆可通过抑制survivin的表达来促进体外培养的EMs异位内膜细胞的凋亡。

Objective To investigate the role of survivin gene in the pathogenesis of endometfiosis（ EMs）. Methods The expressions of survivin in endometriosis and normal endometrium tissue were determined; the effects of GnRHa and COX-2 on the expression of survivin mRNA in endometriosis and normal endometrium in vitro and the effects of GnRHa and COX-2 on the apoptosis index in the cultured ectopic endometrial cells were investigated. Resuits ①The expression of survivin mRNA was higher in patients with endometriosis than that of healthy controls （P 〈 0.01 ） ,with no cyclical variation. ②GnRHa exerted a dose-dependent suppression of survivin mRNA expression in cultured ectopie endometrioma cells as well as COX-2. The significant suppression was observed at the 100 μg/L concentration of GnRHa and at the 40 μmol/L concentration of COX-2. No cooperation was found between them （ P 〉 0.05 ）. Conclusion ①The up-regulation of survivin mRNA expression may reduce the sensitivity of endometriotie cells to apoptosis. Elevated expression of survivin mRNA in ectopic endometrium may have important implications for the survival and proliferation of the ectopie endometrial tissue. ②Both GnRHa and COX-2 can promote apoptosis by inhibiting survivin mRNA expression in eetopic endometrioma cells in vitro.