摘要
目的:探讨米非司酮对子宫内膜单纯性增生的调节机制。方法:正常子宫内膜组织10例(增生期和分泌期各5例),单纯性增生子宫内膜43例,同一患者口服3个月米非司酮(10 mg/d)治疗后的子宫内膜标本43例。采用链酶菌素-生物素(S-P)免疫组化染色方法测定bcl-2、bax的表达量采用SPSS11.5统计学软件包进行数据处理,以P<0.05为有显著性差异。结果:增生期子宫内膜bcl-2阳性信号明显高于分泌期(P<0.05),单纯性增生bcl-2表达明显高于正常增生期子宫内膜(P<0.05)。与单纯性增生相比,米非司酮治疗后,子宫内膜bcl-2明显下降(P<0.05)。分泌期bax表达明显高于增生期(P<0.05),单纯性增生bax表达明显低于正常增生期子宫内膜(P<0.05)。与单纯性增生相比,米非司酮治疗后,子宫内膜bax明显增高(P<0.05)。结论:RU486增加了子宫内膜bax的表达,减少了bcl-2的表达,可能是其促进细胞凋亡,抑制子宫内膜增生的机制之一。
Objective： To explore the adjust mechanism of simple hyperplasia（SH） endometrium treated by mifepristone.Methods： Immunohistochemical SP method was used to measure the expression of bcl-2 and bax in 10 normal endometrium（5 cases proliferative endometrium and secretory endometrium respectively）,43 SH and 43 endometrium after treatment with mifepristone.Results： The expression of bcl-2 in proliferative endometrium（PE） was higher than that in secretory endometrium（SE）（P0.05）,and that in SH was higher than that in PE（P0.05）.Compared with SH,the expression of bcl-2 decreased after treatment with mifepristone（P0.05）.The expression of bax in SE was higher than that in PE（P0.05）,and that in SH was lower than in PE（P0.05）.Compared with SH,the expression of bax increased after treatment with mifepristone（P0.05）.Conclusion： Mifepristone induced bax levels,while suppressing bcl-2 levels.The ability of mifepristone probably promote cellular apoptosis,which was one of the reasons to reduce endometrial hyperplasia.
出处
《生殖与避孕》
CAS
CSCD
北大核心
2011年第5期335-338,共4页
Reproduction and Contraception
