失控的子宫内膜氧化应激和慢性炎症是反复胚胎移植失败、自然流产和不孕的共同病理环节。然而，已知的氧自由基（ROS）和炎性介质的作用并不能完全解释所有的胚胎和子宫内膜之间的容受失败。显然，尚有其他未知的蛋白分子信号途径参与了这个复杂的生理过程。一直以来，雄激素在不孕中的作用大多被认为是以负面为主而一度被忽视。然而，近年的研究发现，脱氢表雄酮（DHEA）作为一种有抗氧化活性的雄激素，不仅参与胚胎着床，而且与子宫内膜的蜕膜化过程紧密相关，但具体的机制并不明确，致使其某些临床应用缺乏足够的依据并可能留下未知的隐患。本项目拟使用DHEA干预体外共培养的小鼠胚胎+子宫内膜细胞氧化应激模型，通过蛋白组学分析，比较DHEA干预组和非干预组之间的相关蛋白表达差异，旨在探讨子宫内膜容受性形成可能的分子机制，为临床不孕症的治疗提供实验依据及新的线索。

Uncontrolled endometrial oxidative stress and chronic inflammation are the common pathological processes for repeated embryo implantation failure, spontaneous abortion and infertility. However, the unsuccessful reception of embryo by the endometrial membrane can not be fully explained by the effects of known classical reactive oxygen species (ROS) and inflammatory cytokines, implying that other unrevealed protein molecular signal pathways may also have been involved in this complicated process. In the past decades, the negative effect of androgen has been highlighting in infertility and it was once neglected. However, recently, a line of evidence have showed that dehydroepiandrosterone (DHEA), a typical androgen with considerable antioxidant capacity, has not only participated in the implantation of embryo but also tightly related to the endometrial decidualization, leaving unclear mechanisms behind. This has limited its administration clinically due to unpredictable side effects. In the current project, using proteomic analysis, we are planning to explore the possible expressing difference of relevant proteins on an in vitro mouse model of oxidative stressed endometrial cells co-cultured with embryos under the exposure of DHEA, expecting to give insights into the possible underlying molecular mechanisms of the endometrial receptivity and to provide research data and new clues for the treatment of infertility.