石榴果提取物对子痫前期血浆内皮细胞血管紧张素- ii型受体和凝血素B2的抑制作用

Widyayu Kusumawati, K. Keman, Setyawati Soeharto
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引用次数: 4

摘要

本研究旨在探讨石榴果提取物对子痫前期患者血浆诱导内皮细胞中血管紧张素- ii型受体(AT1-R)和血栓素B2水平的调节作用。内皮细胞来源于人脐血管内皮细胞。在合流时,内皮细胞被分为五组,包括暴露于2%正常妊娠血浆(NP)的内皮细胞,暴露于2%子痫前期患者血浆(PP)的内皮细胞,以及暴露于存在石榴醇提取物(PP + PG)的PP的内皮细胞,剂量为以下三种:14;28日;56 ppm。免疫组化法检测AT1-R表达,免疫分析法检测血栓素B2水平。与正常妊娠血浆处理的细胞相比,PP血浆显著增加了AT1-R表达和血栓素B2水平。高剂量石榴提取物显著抑制了AT1-R表达的升高(P < 0.05)。最低剂量石榴提取物显著降低了小鼠血栓素B2水平的升高(P < 0.05)。我们进一步得出结论,石榴果通过抑制AT1-R表达(56 ppm)和降低血栓素B2水平(14 ppm)来保护和抑制内皮细胞对子痫前期患者血浆的敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inhibitory Effect of the Punica granatum Fruit Extract on Angiotensin-II Type I Receptor and Thromboxane B2 in Endothelial Cells Induced by Plasma from Preeclamptic Patients
This study aims to evaluate whether the Punica granatum fruit extract modulates the Angiotensin-II Type I receptor (AT1-R) and thromboxane B2 level in endothelial cells induced by plasma from preeclamptic patients. Endothelial cells were obtained from human umbilical vascular endothelial cells. At confluence, endothelial cells were divided into five groups, which included endothelial cells exposed to 2% plasma from normal pregnancy (NP), endothelial cells exposed to 2% plasma from preeclamptic patients (PP), and endothelial cells exposed to PP in the presence of ethanolic extract of Punica granatum (PP + PG) at the following three doses: 14; 28; and 56 ppm. The expression of AT1-R was observed by immunohistochemistry technique, and thromboxane B2 level was done by immunoassay technique. Plasma from PP significantly increased AT1-R expression and thromboxane B2 levels compared to cells treated by normal pregnancy plasma. The increasing of AT1-R expression significantly (P < 0.05) attenuated by high dose treatments of Punica granatum extract. Moreover, the increasing of thromboxane B2 levels significantly (P < 0.05) attenuated by lowest dose treatments of Punica granatum extract. We further concluded that Punica granatum fruit protects and inhibits the sensitivity of endothelial cells to plasma from preeclamptic patients due to inhibition of AT1-R expression (56 ppm) and reduced thromboxane B2 levels (14 ppm).
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