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子宫内膜异位症细胞雌激素与芳香化酶表达的研究

         

摘要

目的检测芳香化酶与雌激素在子宫内膜异位症(简称内异症)细胞中的表达及其作用.方法建立体外原代培养内异症子宫内膜细胞系13份,异位病灶基质细胞系5份,非内异症内膜细胞系6份.采用化学发光法检测细胞上清液中雌二醇的表达水平,应用蛋白印迹法和RT -PCR的方法观察在原代培养子宫内膜异位症内膜细胞、异位病灶细胞以及对照组内膜细胞中的芳香化酶表达情况,以及生理药物浓度的雌二醇刺激原代培养子宫内膜异位症子宫内膜细胞、异位病灶细胞时芳香化酶的表达.结果统计分析显示三组培养细胞上清液的雌二醇表达无显著差异.内异症子宫内膜与异位基质细胞全部表达芳香化酶,而非内异症子宫内膜细胞很少或极低水平表达(P<0.001).芳香化酶mRNA的表达在培养内异症子宫内膜低于异位基质细胞,但显著高于非内异症子宫内膜细胞(P<0.001).雌二醇可以显著增加培养内异症细胞芳香化酶及其转录刺激因子SF-1蛋白与mRNA表达.结论子宫内膜细胞异常表达芳香化酶可以认为是内异症发生、发展的根源之一;雌激素能促进体外培养内异症内膜细胞与异位基质细胞芳香化酶的表达.%Objective To detect the expression and function of aramatase and estradiol in primary cultured cells from endometrio-sis .Methods Thirteen endometrial cells from endometriosis patients (EM ) ,six from non-endometriosis patients (nonEM ) ,and five stromal cells from ectopic endometriotic implants (EC) were primarily cultured in vitro successfully .The estradiol expressions in cul-ture-supernatants were investigated by chemical luminescence method .The expression of aromatase and its messager RNA (mRNA) in those cultured cells were tested by semi-quantitative western blotting and reverse transcription polymerase chain reaction (RT -PCR) .Furthermore ,Cell were stimulated with estradiol and blank respectively .The expression of aromatase and its messager RNA (mRNA) in those cultured cells were detected .Results There were no statistical differences in the expression of estradiol among those culture-supernatants .In groups of EM and EC cells ,the positive rate for aromatase were 100% ,but seldom detectable in cells of nonEM .There were remarkable differences among the relative levels of aromatase of three groups ( P<0 .001) .EM cells and EC cells stimulated by Estradiol can express aromatase mRNA and release aromatase in a dose-dependent fashion .Conclusions The ex-pression of aromatase was stronger in ectopic stromal cells of endometriosis .It may be the crux for the implantation and growth of en-dometriotic lesions .Estradiol can increase the expression of aromatase in cultured endometrial cells from endometriosis patients .

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