内皮细胞中血管紧张肽Ⅱ对内皮型一氧化氮合酶表达的影响

被引：1

作者：

杨丽霞

郭瑞威

石燕昆

齐峰

郭传明

机构：

[1] 成都军区昆明总医院心内科

来源：

中国急救医学 | 2006年 / 01期

关键词：

血管紧张肽Ⅱ; 内皮型一氧化氮合酶; 人脐静脉内皮细胞; 核因子-κB;

D O I：

暂无

中图分类号：

R363 [病理生理学];

学科分类号：

100104 ;

摘要：

目的探讨在内皮细胞中血管紧张肽Ⅱ(AngⅡ)对内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)表达的影响以及AT1、AT2和核因子-κB(NF-κB)在其中的作用。方法体外培养人脐静脉内皮细胞,用AngⅡ单独和与缬沙坦(AT1的抑制剂)、PD123319(AT2的抑制剂)、PDTC(NF-κB的抑制剂)联合干预细胞后,用RT-PCR检测eNOS mRNA表达,Western blot检测eNOS蛋白表达,EMSA检测NF-κB的活性。结果在AngⅡ干预2 h后NF-κB活性增强(P<0.05),PDTC和缬沙坦可以抑制活性的增强,而PD123319则无此作用;5 h后eNOS的mRNA和蛋白表达下调(P<0.05),缬沙坦能抑制这种下调(P<0.05),PDTC无此作用,PD123319作用后eNOS的表达进一步下调,但与AngⅡ组无显著差别。结论在内皮细胞中AngⅡ与AT1结合后,可以导致NF-κB的激活和eNOS表达的下调,而NF-κB通路并没参与到AngⅡ对eNOS的调控中。

引用

页码：34 / 36

页数：3

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