G-蛋白耦联受体30调控一氧化氮合成与子痫前期的关系
发布时间:2018-10-18 21:24
【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(P0.01,P0.05);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(P0.01,P0.05),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(P0.01,P0.05)。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。
[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粏鑳炴ā鍨嬩腑,GPR30,p-eNOS(Ser1177)鍦℉/R缁勪腑鐨勮〃杈捐緝N缁勬樉钁楅檷浣,
本文编号:2280394
[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粏鑳炴ā鍨嬩腑,GPR30,p-eNOS(Ser1177)鍦℉/R缁勪腑鐨勮〃杈捐緝N缁勬樉钁楅檷浣,
本文编号:2280394
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