中文摘要：

目的：探讨G-蛋白耦联受体30（GPR30）调控一氧化氮（NO）合成的信号通路,及其与子痫前期（PE）发病的关系。方法：用免疫组化法检测GPR30在PE组（22例）及正常产妇对照组（N组,21例）的胎盘及蜕膜组织中的表达。以蛋白印迹技术检测GPR30、p-eNOS（Ser1177）、PI3K（p-p85）、p-Akt（Ser473）在经过缺氧/复氧（H/R）、GPR30激动剂（E2或者G1）以及GPR30抑制剂（G15）处理后细胞模型中的表达。结果：GPR30在PE组胎盘、蜕膜组织中表达均较N组显著降低;在细胞模型中,GPR30、p-eNOS（Ser1177）在H/R组中的表达较N组显著降低（P〈0.01,P〈0.05）;GPR30激动剂E2或者G1预处理后,GPR30、p-eNOS（Ser1177）、PI3K（p-p85）、p-Akt（Ser473）在H/R＋E2组和H/R＋G1组的表达均较H/R组上调（P〈0.01,P〈0.05）,而GPR30抑制剂G15作用则相反：GPR30、p-eNOS（Ser1177）、PI3K（p-p85）、p-Akt（Ser473）在H/R＋E2＋G15组的表达均较H/R＋E2组降低（P〈0.01,P〈0.05）。结论：在PE患者胎盘及蜕膜中,GPR30表达下降可能通过PI3K/Akt通路下调NO合成。

英文摘要：

Objective：To explore the effects of g-protein coupled receptor 30（GPR30）on the production of nitric oxide（NO）,as well as the relationship with preeclampsia（PE）.Methods：Immunohistochemistry was used to detect the expression of GPR30 in the placental,decidua tissues of PE（22cases,PE group）or normal pregnant women（21cases,control group）.Western blotting was used to detect the expression of GPR30,p-eNOS（Ser1177）,PI3K（p-p85）and p-Akt（Ser473）protein in hypoxia/reoxygenation（H/R）,GPR30 agonists or GPR30 inhibitor treatment groups of cell model.Results：The expression of GPR30 in placental vascular endothelial cells was lower in placentas,decidua tissues of PE than that of normotensive controls（P〈0.01,P〈0.05）.In the cell model,after（H/R）treatment,the expression of GPR30 and p-eNOS（Ser1177）were significantly lower than those of control group（P〈0.01,P〈0.05）;while with the GPR30 agonists E2or G1 pretreatment,the expression of GPR30、p-eNOS（Ser1177）、PI3K（p-p85）and p-Akt（Ser473）in H/R＋E2or H/R＋G1groups significantly increased when compared with H/R group（P〈0.01,P〈0.05）,while the GPR30 inhibitor G15had the opposite effects,the expression of GPR30、p-eNOS（Ser1177）,PI3K（p-p85）and p-Akt（Ser473）in H/R＋E2＋G15groups decreased when compared with H/R＋E2group（P〈0.01,P〈0.05）.Conclusions：GPR30is an important regulator of the NO production in the placenta and deciduas of PE patient,the decreased expression of GPR30 may down-regulation of NO through the PI3K/Akt pathway.