Investigation on the role of oxidative stress on placental dysfunction and trophoblast function

本研究旨在阐明XO产生的活性氧（reactive oxygen species，ROS）对绒毛外滋养层细胞（extravillous trophoblast，EVT）的生物学影响，探讨EVT功能在子痫前期发病机制中的可能作用。X/XO通过H_2O_2的产生抑制细胞生长，显著增加尿酸水平和凋亡细胞比例。HT前组的平均出生体重显著较低，与标准出生体重的负偏差较大。妊娠32周后DBP升高是SGA的危险因素。妊娠28-30周后，妊高征发生率差异有统计学意义。总之，XO产生的ROS诱导细胞凋亡，影响EVT的功能，包括侵袭和分化。我们最近在日本的一个人口数据库的临床数据可以加强流行病学证据，滋养层细胞的入侵是相关的妊高征的发病机制。

This study was aim to clarify the biological influence of reactive oxygen species (ROS) produced by XO on extravillous trophoblast (EVT) cell and investigate possible role of the EVT function ion the pathogenesis of preeclampsia. X/XO decreased the cell growth by H2O2 produciton, increased the urate level and the apoptotic cell ratio significantly. The Pre-HT group had a significantly lower mean birth weight and a larger negative deviation from the standard birth weight. The DBP elevation after 32 weeks of gestation was a risk factor for SGA. After 28-30 weeks, there was a statistically significant difference in the incidence of PIH. In conclusion, ROS produced by XO induced apoptosis and affected EVT function including invasion and differentiation. Our clinical data from a recent population database in Japan could strengthen epidemiologic evidence that trophoblast invasion is related to the pathogenesis of PIH.