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目的研究17β-雌二醇(17β-E2)对子宫内膜异位症(内异症)患者在位子宫内膜间质细胞β-catenin mRNA和蛋白表达的影响,探讨Wnt/β-catenin信号通路在介导雌激素促进内异症发生发展的作用。方法体外分离培养内异症患者在位子宫内膜间质细胞。用不同浓度17β-E2处理子宫内膜间质细胞48 h;此后选用10-10mol/L 17β-E2处理子宫内膜间质细胞12、24和48 h,逆转录聚合酶链反应(RT-PCR)和免疫印迹法(Western blotting)检测17β-E2处理前后子宫内膜间质细胞β-catenin mRNA和蛋白的表达水平。同法分析雌激素受体拮抗剂ICI182,780(10-6mol/L)对17β-E2促进β-catenin mRNA和蛋白表达的影响。免疫组织化学染色观察17β-E2作用后β-catenin在子宫内膜间质细胞中的定位。结果17β-E2能明显促进内异症患者在位子宫内膜间质细胞β-catenin mRNA和蛋白的表达,并呈剂量和时间依赖性,于10-10mol/L作用48 h最明显。雌激素受体拮抗剂ICI182,780能明显抑制17β-E2对子宫内膜间质细胞β-catenin mRNA和蛋白的表达。免疫组织化学染色发现17β-E2能促进β-catenin在子宫内膜间质细胞核内的表达。结论雌激素可能通过激活Wnt/β-catenin信号通路促进内异症在位子宫内膜的异位种植。
Objective To investigate the effect of 17β-estradiol (17β-E2) on the expression of β-catenin mRNA and protein in endometriotic stromal cells in patients with endometriosis (endometriosis) and to explore the role of Wnt / β-catenin signaling Pathway mediates the role of estrogen in promoting the development of endometriosis. Methods In vitro culture of endometriosis stromal cells in patients with endometriosis. Endometrial stromal cells were treated with different concentrations of 17β-E2 for 48 h. Afterwards, endometrial stromal cells were treated with 10-10 mol / L 17β-E2 for 12, 24 and 48 h respectively, and RT-PCR ) And Western blotting were used to detect the expression of β-catenin mRNA and protein in endometrial stromal cells before and after treatment with 17β-E2. The same method was used to analyze the effect of estrogen receptor antagonist ICI182,780 (10-6mol / L) on the expression of β-catenin mRNA and protein by 17β-E2. Immunohistochemical staining was used to observe the localization of β-catenin in endometrial stromal cells after 17β-E2 treatment. Results 17β-E2 could significantly promote the expression of β-catenin mRNA and protein in endometriotic stromal cells in a dose-and time-dependent manner. Estrogen receptor antagonist ICI182,780 can significantly inhibit the expression of β-catenin mRNA and protein of 17β-E2 on endometrial stromal cells. Immunohistochemical staining revealed that 17β-E2 promoted the expression of β-catenin in endometrial stromal cells. Conclusion Estrogen may promote ectopic implantation of endometriosis by activating Wnt / β-catenin signaling pathway.