【摘要】：目的:探討G-蛋白耦聯(lián)受體30(GPR30)調(diào)控一氧化氮(NO)合成的信號通路,及其與子癇前期(PE)發(fā)病的關(guān)系。方法:用免疫組化法檢測GPR30在PE組(22例)及正常產(chǎn)婦對照組(N組,21例)的胎盤及蛻膜組織中的表達。以蛋白印跡技術(shù)檢測GPR30、p-eNOS(Ser1177)、PI3K(p-p85)、p-Akt(Ser473)在經(jīng)過缺氧/復氧(H/R)、GPR30激動劑(E2或者G1)以及GPR30抑制劑(G15)處理后細胞模型中的表達。結(jié)果:GPR30在PE組胎盤、蛻膜組織中表達均較N組顯著降低;在細胞模型中,GPR30、p-eNOS(Ser1177)在H/R組中的表達較N組顯著降低(P0.01,P0.05);GPR30激動劑E2或者G1預處理后,GPR30、p-eNOS(Ser1177)、PI3K(p-p85)、p-Akt(Ser473)在H/R+E2組和H/R+G1組的表達均較H/R組上調(diào)(P0.01,P0.05),而GPR30抑制劑G15作用則相反:GPR30、p-eNOS(Ser1177)、PI3K(p-p85)、p-Akt(Ser473)在H/R+E2+G15組的表達均較H/R+E2組降低(P0.01,P0.05)。結(jié)論:在PE患者胎盤及蛻膜中,GPR30表達下降可能通過PI3K/Akt通路下調(diào)NO合成。
[Abstract]:Aim: to investigate the effect of G-protein coupled receptor 30 (GPR30) on nitric oxide (NO) synthesis and its relationship with preeclampsia (PE). Methods: immunohistochemical method was used to detect the expression of GPR30 in placenta and decidua of PE group (22 cases) and normal control group (21 cases). The expression of GPR30,p-eNOS (Ser1177), PI3K (p-p85) and p-Akt (Ser473) was detected by Western blot in the cell model after hypoxia / reoxygenation (H / R), GPR30 agonist (E _ 2 or G _ 1) and GPR30 inhibitor (G15). Results: the expression of GPR30 in placenta and decidua of PE group was significantly lower than that in N group. 鍦ㄧ粏鑳?yōu)妯″瀷涓?GPR30,p-eNOS(Ser1177)鍦℉/R緇勪腑鐨勮〃杈捐緝N緇勬樉钁楅檷浣，

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