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子痫前期由于胎盘的缺血缺氧,使胎盘来源的“毒性因子”过多的进入母体循环,导致相应受体的表达增多及激活,使内皮细胞内活性氧的产生增多,一氧化氮的灭活增加。活性氧作为细胞内的第二信使激活转录因子NFκ-B,导致炎症相关基因的表达,促使中性粒细胞黏附,造成内皮炎性损伤;同时循环中促损伤后修复的作用削弱,进一步加剧了内皮损伤。
Because of placental ischemia and hypoxia in preeclampsia, placenta-derived “toxic factor” into the maternal circulation too much, leading to increased expression and activation of the corresponding receptors, so that the production of reactive oxygen species in endothelial cells, nitric oxide Inactivation increased. Reactive oxygen species activate the transcription factor NFκ-B as the second messenger in cells, leading to the expression of inflammation-related genes, promoting the adhesion of neutrophils, resulting in inflammatory injury of the endothelium; meanwhile, the role of post-injury repair in circulation is weakened, further aggravating Endothelial damage.