子痫前期（PE）是常见的妊娠期并发症。胎盘滋养细胞分化障碍、侵袭相关因子表达失衡是导致PE胎盘螺旋动脉重铸不良的重要原因。PE胎盘存在明显内质网应激。已经明确，过度内质网应激可导致细胞功能障碍。晚期氧化蛋白产物（AOPP）是一种具有高度生物活性的代谢产物，可引起细胞内质网应激。课题组前期研究发现AOPP在PE胎盘、血浆表达升高，并与患者病情严重程度密切相关。我们推测 AOPP 蓄积介导的内质网应激可能引起胎盘滋养细胞分化障碍、侵袭相关因子表达失衡，并导致子痫前期发生风险增加。本项研究我们通过动物实验，观察慢性AOPP 蓄积对妊娠大鼠胎盘内质网应激、滋养细胞分化以及子痫前期发生的影响。同时我们用不同浓度AOPP 刺激人早孕胎盘绒毛，观察其对胎盘内质网应激、滋养细胞分化和侵袭相关因子表达的影响，并探讨 AOPP诱导胎盘滋养细胞分化功能障碍和侵袭相关因子产生失衡可能的受体途及信号通路。

Preeclampsia was a common pregnancy complication. Impaired differentiation of trophoblasts and imbalanced expression of invasive factors were major contributors to spiral arteries remodelling disturbance in preeclampsia. Excessive endoplasmic reticulum stress, which could induce cellular dysfunction, has been observed in preeclampsia placenta. Advanced oxidation protein products (AOPP) were one metabolite, which could induce excessive endoplasmic reticulum stress. We have showed patients with preeclampsia had a higher plasma and placental levels of AOPP. Moreover, the AOPP levels were associated with the severity of the disease. We proposed AOPP might be a novel substance which could cause impaired placental development and onset of preeclampsia. In this study, we explored the effect of AOPP on the rat placental endoplasmic reticulum stress level, placental development as well as the rate of preeclampsia. In addition, placental explants were incubated with various concentrations of AOPP. The effect of AOPP on the endoplasmic reticulum stress level, differentiation of trophoblasts and expression of invasive factors were investigated.