替米沙坦对血管紧张素II诱导的心肌肥大的作用及可能机制  

Effects and Mechanisms of Telmisartan to Inhibit Angiotensin II-Induced Cardiac Hypertrophy in Vitro

作　　者：唐跃东[1] 刘国平[1] 胡朝晖[2] 

机构地区：[1]复旦大学附属金山医院,200540 [2]同济大学附属同济医院心内科,200065

出　　处：《中国分子心脏病学杂志》2011年第2期65-68,共4页Molecular Cardiology of China

摘　　要：目的探讨替米沙坦对血管紧张素II(AngII)诱发的肥大心肌细胞膜AT1和AT2受体表达变化的影响。方法体外培养心肌细胞,分为三组:对照组,AngII处理组,替米沙坦处理组。构建AngII诱发心肌细胞肥大模型,提取各组心肌细胞膜蛋白,免疫印记(Western Blotting)观察肥大心肌细胞中AT1和AT2表达。结果相对于对照组,AngII处理组心房利钠肽(ANP),脑钠肽(BNP)基因表达明显上升(P<0.05),AT1和AT2受体表达也显著上升(P<0.05);相对于AngII组,替米沙坦处理组ANP,BNP基因和AT1受体表达明显下降(P<0.05)。结论替米沙坦可以明显抑制AngII诱发的心肌细胞肥大,其机制与其降低因AngII诱发AT1受体表达升高和维持AngII引起的AT2受体高表达有关。Objective To observe the changes of AT1 and AT2 expressions in hypertrophic cardiomyocytes induced by Angiotensin II (AngII). Methods Rat neonatal cardiomyocytes were cultured and randomly divided into three groups: control group, AngII group, Telmisartan group. The hypertrophic model of cardiomyocytes evoked by AngII was achieved. Then cardiomyocytes of each group were isolated and collected after treatment with AngII or Telmisartan. The AT1 and AT2 expressions were detected using Western Blot. Results: Co...

关 键 词：心肌细胞 替米沙坦 血管紧张素II1型受体 血管紧张素II2型受体 

分 类 号：R965[医药卫生—药理学]