血红素加氧酶1与子痫前期发病机制的研究进展

被引：6

作者：

刘玲艳

张学勤

机构：

[1] 昆明医科大学第二附属医院产科

来源：

国际妇产科学杂志 | 2015年 / 42卷 / 01期

关键词：

先兆子痫; 血红素氧化酶(脱环); 内皮细胞; 氧化性应激;

D O I：

暂无

中图分类号：

R714.244 [];

学科分类号：

摘要：

子痫前期是妊娠期最常见的疾病之一,其不仅能导致胎盘早剥、妊娠妇女肝肾功能受损、早产、胎儿生长受限等,也是孕产妇及围生儿死亡的常见原因,由于其严重危害母儿健康,其发病机制一直是产科领域的研究热点。子宫螺旋动脉重塑障碍、血管内皮受损、遗传、免疫失衡及炎症反应等与子痫前期关系密切,其中广泛的血管内皮受损是该病发生的关键环节。近年研究发现,氧化应激及可溶性血管内皮因子(s Eng)、可溶性血管内皮生长因子受体1(s Flt-1)升高是导致血管内皮受损的主要原因,而血红素加氧酶1(HO-1)是一种可诱导的抗氧化酶,HO-1及其催化代谢产物一氧化碳(CO)、胆红素不仅对正常妊娠的胎盘形成、胎盘功能的维持及胎儿的生长发育具有重要保护作用,还能通过激活胎盘保护型信号通路、合成还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)还原酶来抑制子痫前期妇女体内的氧化应激以及通过降低血管内皮损伤因子如s Eng、s Flt-1对血管内皮的损害、促进血管内皮保护因子如血管内皮生长因子(VEGF)对血管的保护作用来抑制子痫前期的发生,推测HO-1及其催化代谢产物能够为子痫前期预防及治疗带来新的突破。

引用

页码：65 / 68

页数：4

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