氧化应激在子痫前期发病机制中的作用。

C A Hubel
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引用次数: 634

摘要

妊娠综合征先兆子痫的病因和发病机制尚不清楚。大量证据表明,子痫前期的多种表现,包括血管反应性改变、血管痉挛和许多器官系统的离散病理,都源于母体血管内皮的病理改变。随着内皮细胞功能障碍的主题强调,这篇综述侧重于氧化应激(一种不平衡倾向于氧化剂超过抗氧化剂的力量)在子痫前期发病机制中的作用。资料总结如下:1)胎盘在子痫前期的作用;2)氧化应激在子痫前期胎盘中的作用证据及机制;3)母体循环氧化应激标志物;4)母体血脂异常在氧化应激产生中的潜在作用。一个反复出现的主题是,由病变胎盘和母亲血脂异常之间的“串扰”促进的自由基反应,促进了恶性循环的事件,使因果难以区分,但可能有助于先兆子痫的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress in the pathogenesis of preeclampsia.

The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is substantial evidence to suggest that the diverse manifestations of preeclampsia, including altered vascular reactivity, vasospasm, and discrete pathology in many organ systems, are derived from pathologic changes within the maternal vascular endothelium. With the theme of endothelial cell dysfunction emphasized, this review focuses on the role of oxidative stress (an imbalance favoring oxidant over antioxidant forces) in the pathogenesis of preeclampsia. Data are summarized regarding 1) the role of the placenta in preeclampsia; 2) evidence and mechanisms of oxidative stress in the preeclampsia placenta; 3) markers of oxidative stress in the maternal circulation; and 4) the potential role of maternal dyslipidemia in generation of oxidative stress. A recurrent theme is that free radical reactions, promoted by "cross-talk" between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.

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