腺苷A1受体在妊娠期高血压以及子痫前期中的作用

发布时间：2018-05-11 10:24

本文选题：腺苷A受体 + 子痫前期　；参考：《第二军医大学学报》2017年03期

【摘要】：目的探讨腺苷A1受体(A1R)在妊娠期高血压以及子痫前期发病机制中的作用。方法取剖宫产分娩的妊娠期高血压(n=6)、子痫前期(n=14)和正常对照(n=15)产妇胎盘组织,采用免疫荧光检测A1R在胎盘组织中的表达部位,蛋白质印迹法检测A1R在胎盘中的表达量。建立常氧、缺氧(8、24、48、72h)以及缺氧复氧(8h)滋养细胞模型,运用实时荧光定量PCR和蛋白质印迹法检测A1R在细胞中的表达情况,Transwell和蛋白质印迹法检测加入A1R拮抗剂8-环戊基-1,3-二丙基黄嘌呤(DPCPX)后对缺氧的胎盘滋养细胞侵袭性和蛋白激酶A(PKA)表达的影响。结果 A1R在胎盘表面的滋养细胞以及内皮细胞中均有表达。与正常胎盘比较,A1R在轻度和重度子痫前期胎盘组织中表达升高(P0.01)。A1R在体外胎盘滋养细胞缺氧模型中的表达随着缺氧时间的延长而逐渐升高(P0.05)。胎盘滋养细胞缺氧模型中滋养细胞的侵袭能力较正常组下降(P0.01),PKA表达下降(P0.05);加入拮抗剂DPCPX可以增强滋养细胞的侵袭性(P0.05),同时上调PKA的表达水平(P0.05)。结论缺氧程度的增加可以使A1R表达升高,A1R在胎盘滋养细胞中的作用机制可能与调节PKA相关。
[Abstract]:Objective to investigate the role of adenosine A 1 receptor A 1 R in the pathogenesis of hypertension complicating pregnancy and preeclampsia. Methods the placenta tissues of pregnant women with hypertension complicating pregnancy during cesarean section were collected. The expression of A1R in placenta was detected by immunofluorescence, and the expression of A1R in placenta was detected by Western blot. The model of trophoblastic cells was established with normoxic oxygen, anoxic anoxia and anoxic reoxygenation for 72h) and anoxia reoxygenation for 8h). The expression of A1R in human placental trophoblast cells was detected by real-time fluorescence quantitative PCR and Western blotting. Transwell and Western blotting were used to detect the invasiveness of placental trophoblastic cells induced by hypoxia by adding 8-cyclopentyl-1-dipropylxanthine 3- dipropylxanthine into A1R antagonist. And protein kinase (PKA) expression. Results A 1R was expressed in trophoblast and endothelial cells. Compared with normal placenta, the expression of A1R in placenta of mild and severe preeclampsia was higher than that of normal placenta. The invasion ability of trophoblast in placental trophoblastic hypoxia model was lower than that in normal group, and the expression of P0.05A was decreased in placental trophoblastic hypoxia model, and the level of PKA expression was up-regulated by adding antagonist DPCPX to enhance the invasiveness of trophoblast. Conclusion the increase of hypoxia may increase the expression of A1R in placental trophoblastic cells and its mechanism may be related to the regulation of PKA.
【作者单位】：重庆医科大学附属第二医院妇产科;重庆医科大学附属第一医院妇产科;
【分类号】：R714.24

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