PPARγ激动剂抑制AngⅡ诱导乳鼠心肌细胞合成肿瘤坏死因子  

PPARγ activators inhibitory effects on angiotensinⅡ induced tumor necrosis factora expression in neonatal rat cardiac myocytes

作　　者：汪华玲[1] 覃数[1] 陈齐红[1] 

机构地区：[1]重庆医科大学临床学院心内科,重庆400016

出　　处：《重庆医科大学学报》2005年第3期373-375,共3页Journal of Chongqing Medical University

摘　　要：目的:研究过氧化体增殖物激活型受体γ(PPARγ)激动剂(罗格列酮)对血管紧张素Ⅱ(AngⅡ)刺激乳鼠心肌细胞合成肿瘤坏死因子(TNF-α)的影响,旨在探讨罗格列酮作用于心肌细胞时,在细胞因子调节中发挥的作用。方法:采用酶消化和差速贴壁法分离乳鼠心肌细胞。罗格列酮预处理30min后,用AngⅡ与乳鼠心肌细胞共同培养24h,然后分别采用ELISA和RT-PCR法检测细胞培养上清液TNF-α含量和心肌细胞TNF-αmRNA表达水平。结果:AngⅡ刺激乳鼠心肌细胞TNF-α蛋白质合成和mRNA表达增加,罗格列酮抑制AngⅡ的作用(P<0.01),且在一定范围内,浓度越高作用越强。结论:罗格列酮抑制AngⅡ刺激的乳鼠心肌细胞TNF-αmRNA表达和蛋白质合成,罗格列酮这一作用为治疗慢性心力衰竭提供了新的思路。Objective:To explore the effects of the nuclear receptor peroxisome proliferator-activated receptor (PPAR)γ activators on tumor necrosis factor α (TNF-α) expression in neonatal rat cardiac myocytes.Methods:Primary culture of cardiac myocytes was prepared from 1～3 days old Spraque-Dawley rats.Cardiac myocytes were pretreated with rosiglitazone at different concentrations and then stimulated with angiotensin Ⅱ(1 μmol/L).ELISA and reverse transcripition-polymerase chain reaction(RT-PCR) were used to examine TNF-α in cultured supernatants and TNF-α mRNA in cardiac myocytes,respectively.Results:Pretreatment of cardiac myocytes with rosiglitazone inhibited the increase of TNF-α and TNF-α mRNA induced by angiotensinⅡ in a concentration-dependent manner.Conclusion:Rosiglitazone inhibits the expression of TNF-α in cardiac myocytes,which provides a new way for treating chronic heart failure.

关 键 词：过氧化体增殖物激活型受体Γ TNF—α AngⅡ 心肌细胞 

分 类 号：R541[医药卫生—心血管疾病]