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目的:米非司酮用于子宫肌瘤治疗效果较好,但目前机制不明,本研究中探讨米非司酮治疗子宫肌瘤的可能机制。方法:获取手术组织标本和分离子宫肌瘤细胞,采用Western blot方法研究雌激素受体(ER)和血管内皮生长因子受体(VEGFR)的表达水平,采用RNA干扰方法研究ER表达沉默后VEGFR的表达改变,采用MTT法研究米非司酮对子宫肌瘤细胞的生长抑制作用。结果:子宫肌瘤组织中ER及VEGFR的表达水平明显高于肌瘤周围正常子宫肌组织,差异具有统计学意义,并且肌瘤组织中ER和VEGFR的表达有正相关性。RNA干扰方法沉默子宫肌瘤细胞中ER表达后VEGFR的表达水平降低。米非司酮对VEGFR表达水平较高的子宫肌瘤细胞具有较强的生长抑制作用,而且经米非司酮作用后子宫肌瘤细胞的PR、ER和VEGFR表达水平降低。结论:米非司酮可能通过ER、PR和VEGFR途径发挥抑制子宫肌瘤生长的作用。
Objective: Mifepristone for the treatment of uterine fibroids better, but the mechanism is unknown, the study to explore the possible mechanism of mifepristone treatment of uterine fibroids. Methods: The specimens of the surgical tissue were collected and the uterine fibroids were isolated. The expression of estrogen receptor (ER) and vascular endothelial growth factor receptor (VEGFR) was detected by Western blot. The expression of VEGFR The expression of Mifepristone on the growth inhibition of uterine fibroids was studied by MTT assay. Results: The expression of ER and VEGFR in uterine fibroids was significantly higher than that in normal uterine muscle tissue around fibroids, the difference was statistically significant, and the expression of ER and VEGFR in myoma was positively correlated. The RNA interference method silenced the expression of VEGFR in uterine fibroids after ER expression. Mifepristone has a strong growth inhibitory effect on uterine myoma cells with higher VEGFR expression, and the expression of PR, ER and VEGFR in uterine fibroids decreased after mifepristone treatment. Conclusion: Mifepristone may exert inhibitory effects on the growth of uterine fibroids through ER, PR and VEGFR pathways.