米非司酮对小鼠植入窗期子宫内膜水通道蛋白1的调节及作用机制

米非司酮（mifepristone,RU486）是人类合成的一种19-去甲类固醇，通过竞争性结合孕激素受体，在受体水平特异性阻断孕激素的作用，同时也能与糖皮质激素受体结合而起拮抗作用。目前米非司酮已广泛用于临床终止早期妊娠，也用于紧急避孕的临床研究。近年研究发现，在人子宫内膜中，水通道蛋白-1的表达具有周期性，在植入窗期表达明显增加，对正常妊娠的建立与维持具有重要的作用。因此，我们推测米非司酮可能通过对水通道蛋白-1表达的影响而发挥内膜避孕的作用。 就上述问题，采用体外实验，从细胞和分子水平，利用免疫组化法、real-time PCR、免疫印迹、渗透试验、血管生成试验等相关技术，进一步探讨低剂量米非司酮作为抗着床避孕药可能的机制，为新的避避径的开发以及人类的生殖过程中相关疾病的发生机理和治疗研究提供新的思路。

Mifepristone is an antiprogestin which interacts with progesterone at the receptor level. Mifepristone was the first progesterone receptor (PR) antagonist approved for clinical use and has been used widely as an abortion drug. Currently, mifepristone is used as an emergency contraceptive drug, and it has been found recently that the dosage required for effective contraception is lower than originally suggested, thereby increasing both acceptability and continuation rates. However, the contraceptive mechanisms of mifepristone remain undetermined. AQP1 was most concentrated within the endometrium at the time of implantation, suggesting that AQP1 might play physiological roles in the uterine receptivity. In order to investigate the role of low dose mifepristone as an anti-implantation contraceptive drug, immunohistochemisty and real-time PCR were used to analyze the effects of low dose mifepristone on the expression levels of AQP1 in human endometrium at the time of implantation.