摘要
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。
Owing to ischemia and hypoxia of placenta in eclampsism, the ＂deleterious factors＂ excessively enter the pregnant women＇ s circulation, which may cause the increased expression and activation of their corresponding receptors on endothelial cells, which result in the increasion of the production of active oxygen in cell and the deactivation of NO. Active oxygen as the second messenger can further activate transcription factor NF-kB which then promotes the expression of the inflammatory related genes, promote the adhension of neutrophils and result in endothelial inflammatory damage, meanwhile the impairment of factors promoting repair following injury in circulation will further aggravate the endothelial damage.
出处
《医学综述》
2006年第18期1099-1101,共3页
Medical Recapitulate
关键词
子痫前期
内皮细胞
氧化应激
内皮损伤
Eclampsism
Endothelial cells
Oxidative stress
Endothelial cell injury
