G-蛋白耦联受体30调控一氧化氮合成与子痫前期的关系  被引量:2

G-Protein Coupled Receptor 30 Contacts with Preeclampsia through the Regulation of Nitric Oxide Production

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作  者:周丽媛[1,2] 张华[1,2] 

机构地区:[1]重庆医科大学附属第一医院 [2]重庆医科大学中国-加拿大-新西兰联合母胎医学实验室,重庆400016

出  处:《实用妇产科杂志》2015年第10期753-757,共5页Journal of Practical Obstetrics and Gynecology

基  金:国家自然科学基金资助项目(编号:81100444);重庆市自然科学基金资助项目(编号:2011BB5121);重庆市卫生局科研基金资助项目(编号:2011-2-046)

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。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.

关 键 词:子痫前期 GPR30 血管内皮 一氧化氮 

分 类 号:R714.24[医药卫生—妇产科学]

 

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