子宫腺肌病在位内膜腺上皮细胞中HPA和metastin的表达及米非司酮对其表达的影响  

Heparanase and metastin expressions in eutopic endometrial glandular epithelium cells of adenomyosis in vitro and the effect of mifepristone for their expressions and significance

作　　者：李莉[1] 刘海瑛[1] 张亚琴[1] 张华屏[1] 侯红丽[1] 

机构地区：[1]山西医科大学第一医院妇产科,山西太原030001

出　　处：《中国实用妇科与产科杂志》2009年第9期674-676,共3页Chinese Journal of Practical Gynecology and Obstetrics

基　　金：山西省科技攻关项目(042024-2)

摘　　要：目的探讨米非司酮对子宫腺肌病发病中侵袭性因素的干预机制。方法2007年7月至2008年12月在山西医科大学第一医院经病理诊断为子宫腺肌病患者32例采用反转录-聚合酶链反应(RT-PCR)法和Western-blot法检测其体外培养子宫腺肌病在位内膜腺上皮细胞中乙酰肝素酶(heparanase,HPA)和Kiss-1基因及HPA和转移抑素(metastin)蛋白的表达,并用米非司酮对其进行干预。结果子宫腺肌病组增殖期和分泌期腺上皮细胞中HPA mRNA表达分别为1.39±0.05和1.28±0.04,高于对照组(P<0.05);Kiss-1 mRNA表达分别为0.78±0.07和0.82±0.05,低于对照组(P<0.05),同一组内增殖期和分泌期相比没有统计学意义(P>0.05)。HPA和metastin蛋白表达与基因表达一致。对子宫腺肌病组进行米非司酮药物干预后,HPA mRNA和HPA蛋白表达降低,Kiss-1 mRNA和metastin蛋白表达增高,与未用药前相比有统计学意义(P<0.05)。结论子宫内膜腺上皮细胞中侵袭性因素和侵袭抑制因素表达失衡可能是子宫腺肌病的发病机制之一;米非司酮对HPA和metastin的干预作用可能成为米非司酮抑制子宫腺肌病发展的机制之一。Objective To detect the expression of heparanase, Kiss-1 and metastin in eutopic endometrial glandular cells of adenomyosis in vitro, and the effects of mifepristone on the expression, in order to investigate the effects of mifepristone on the intervention mechanism of invasive factors in adenomyosis. Methods 32 cases of patients were pathologically diagnosed as adenomyosis at the First Hospital of Shanxi Medical University between July 2007 and December 2008, using RT-PCR and Western-blot to detect the HPA and Kiss-1 gene and the HPA and metastin protein expression in eutopic endometrial glandular cells of adenomyosis in vitro, and intervening with mifepristone. Results The expression of HPA mRNA in adenomyosis group proliferative and secretory phase glandular epithelial cells were 1.39±0.05 and 1.28±0.04 respectively, higher than control group （P〈0.05）. Kiss-1 mRNA expression were 0.78±0.07 and 0.82±0.05 respectively, lower than the control group （P〈0.05）. However, there is no statistical significance between proliferative and secretory phase within the same group（P〉0.05）. The levels of protein expression of HPA and metastin showed consistent with the gene expression. After drug intervention on adenomyosis group, HPA mRNA and protein expression decreased, and Kiss-1 mRNA and protein expression metastin increased, which means obvious differences compared to pre-treatment （ P 〈 0.05 ）. Conclusion The imbalance expression of invasive factors （HPA） and invasive inhibiting factors （metastin） in endometrial glandular epithelial cells may be one of the pathogenesis; the intervention of mifepristone on the above two factors may be one of the inhibitive mechanisms on adenomyosis development.

关 键 词：子宫腺肌病 乙酰肝素酶 KISS-1 转移抑素 米非司酮 

分 类 号：R71[医药卫生—妇产科学]