氯沙坦通过降低ADMA水平诱导血管内皮保护作用

被引：6

作者：

陈美芳 ^{[1
]}

谢秀梅 ^{[1
]}

杨天伦 ^{[1
]}

李元建 ^{[2
]}

机构：

[1] 中南大学湘雅医院心内科

[2] 中南大学药学院心血管药理教研室

来源：

中南药学 | 2007年 / 03期

关键词：

氯沙坦; 血管紧张素Ⅱ(AngⅡ); 非对称性二甲基精氨酸(ADMA); 蛋白甲基转移酶(PRMT); 二甲基精氨酸二甲胺水解酶(DDAH); 活化蛋白(AP-1);

D O I：

暂无

中图分类号：

R96 [药理学];

学科分类号：

100602 ; 100706 ;

摘要：

目的本实验拟观察在培养的人脐静脉内皮细胞,氯沙坦对血管紧张素Ⅱ(AngⅡ)诱导的血管内皮活化的保护作用是否与降低非对称二甲基精氨酸(ADMA)水平有关。方法用不同浓度的AngⅡ(10-9～10-6mol.L-1)孵育不同时间(6～48 h),并加入不同浓度的氯沙坦(1、3、10μmol.L-1)预处理1 h,检测细胞培养上清液中的ADMA、一氧化氮(NO)、肿瘤坏死因子(TNF-α)水平,细胞中蛋白甲基转移酶(PRMT)蛋白表达、二甲基精氨酸二甲胺水解酶(DDAH)和活化蛋白(AP-1)活性。结果AngⅡ呈浓度和时间依赖性增加PRMT的表达,AngⅡ(10-6mol.L-1,24 h)显著增加培养液中ADMA、TNF-α水平,减少NO的生成,降低细胞DDAH活性,增加细胞AP-1活性。氯沙坦可拮抗AngⅡ所致的上述效应。结论这些结果提示氯沙坦诱导的血管内皮细胞保护作用可能与降低ADMA水平有关。

引用

页码：193 / 198

页数：6

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