检验医学与临床Issue(16)：2328-2330,3.DOI:10.3969/j.issn.1672-9455.2015.16.012
表没食子儿茶素没食子酸酯对血管紧张素Ⅱ诱导的心肌细胞肥大的抑制作用
Inhibitory effect of EGCG on cardiomyocyte hypertrophy induced by angiotensinⅡ
摘要
Abstract
Objective To investigate the inhibitory effect of epigallocatechin gallate(EGCG) on cardiomyocyte hypertrophy induced by angiotensinⅡ(AngⅡ ) and its potential mechanisms .Methods The primarily cultured car‐diomyocyte AngⅡ(0 .1 μmol/L) from sprague dawley neonatal rats was adopted to induce and prepare the cardio‐myocyte hypertrophy model .The nitric oxide (NO) content ,activity of nitric oxide synthetase (NOS) and Ca2+‐AT‐Pase activity in the supernatant fluid of cardiomyocytes culture after EGCG (0 .5 ,1 .0 ,2 .0μmol/L) intervention were measured .Meanwhile the mRNA expressions of calcineurin (CaN) in cardiomycytes were detected by real time re‐verse transcription‐polymerase chain reaction (RT‐PCR) .The protein expression of calcineurin catalytic subunit (CnA) was detected by Western blot .Results AngⅡ in the blank control group induced significant cardiomyocytes hypertrophy ,intracellular NOS and Ca2+‐ATPase activity decrease ,while CnA protein content and CaN mRNA ex‐pression increase(P< 0 .05) ,different doses of EGCG significantly alleviated Ang Ⅱ‐induced cardiomyocyte hyper‐trophic degree ,increased the activity of NOS and Ca2+‐ATPase ,promoted the NO release ,but down‐regulated CaN mRNA and decreased CnA protein expression(P<0 .05) .Conclusion The mechanism of EGCG inhibiting Ang Ⅱinduced cardiomyocyte hypertrophy could be related with EGCG increasing NO release ,elevating NOS and Ca2+‐AT‐Pase activity ,inhibiting CaN signal transduction pathway and decreasing CnA protein expression .关键词
表没食子儿茶素没食子酸酯/心肌细胞肥大/Ca2+-AT P 酶/一氧化氮合酶/钙调神经磷酸酶Key words
EGCG/cardiomyocyte hypertrophy/Ca2+-ATP/NOS/CaN引用本文复制引用
王晓,陈华..表没食子儿茶素没食子酸酯对血管紧张素Ⅱ诱导的心肌细胞肥大的抑制作用[J].检验医学与临床,2015,(16):2328-2330,3.基金项目
重庆市基础与前沿研究计划项目（cstc2014jcyjA10049）；重庆市卫生和计划生育委员会医学科研项目（20121096）。 （）
