不对称性二甲基精氨酸与早发型重度子痫前期关系的研究进展  

Research progress of the relationship between asymmetric dimethylarginine and early onset severe preeclampsia

作　　者：程汐 刘国成[1] 

机构地区：[1]广东省妇幼保健院妇产科,广州511400

出　　处：《中华妇幼临床医学杂志（电子版）》2015年第3期115-118,共4页Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition)

摘　　要：不对称性二甲基精氨酸(ADMA)是内源性一氧化氮合酶(NOS)抑制剂,可抑制NOS活性,减少一氧化氮(NO)合成,导致血管内皮细胞功能障碍。早发型重度子痫前期(EOSP)存在胎盘形态学异常,而晚发型重度子痫前期(LOSP)则无明显胎盘形态学异常。因此,胎盘发生和形成异常,可能是导致EOSP发生的原因。该病患者胎盘血管内皮细胞的二甲基精氨酸二甲胺水解酶(DDAH2)表达水平下降,使ADMA降解减少;而血浆及胎盘ADMA水平增加,可竞争性抑制NOS活性,导致NO生成减少及其生物利用度降低,发生胎盘病变及胎盘血管内皮细胞功能障碍。由此可见,ADMA与EOSP胎盘病理改变的发生、发展密切相关,并已成为目前研究热点。笔者拟就ADMA在EOSP中的作用及其可能机制进行综述。As an endogenous nitric oxide synthase（NOS）competitive inhibitor,asymmetric dimethylarginine（ADMA）can inhibit the activity of NOS,reduce the synthesis of nitric oxide（NO）and results in endothelial cell dysfunction.Early onset severe preeclampsia（EOSP） exists placental morphological abnormalities,and late onset severe preeclampsia（LOSP）has no obvious placental morphological abnormalities,so the genesis and formation of abnormal placenta may be the cause of EOSP.The dimethylarginine dimethylaminohydrolase（DDHA）2expression level of placental vascular endothelial cells in EOSP patient descended,and cause ADMA degradation reduced.Increased ADMA expression level of plasma and placenta can competitively inhibit NOS activity,resulting in reduction of NO generate and NO bioavailability,causing placental lesions and dysfunction of placental vascular endothelial cells.It can be seen that ADMA is closely related to genesis and development of placental pathological changes in EOSP,and the fields in research of ADMA and EOSP have become a hot research topic now.This paper focused on the role and its possible mechanism of ADMA in EOSP.

关 键 词：不对称性二甲基精氨酸 早发型重度子痫前期 二甲基精氨酸二甲基氨基水解酶 一氧化氮合酶 

分 类 号：R714.244[医药卫生—妇产科学]