硫氧环蛋白过氧化物酶3对血管紧张素Ⅱ诱导心肌肥大的影响  

Effect of Peroxiredoxin-3 on angiotensin Ⅱ-induced cardiomyocytes hypertrophy

作　　者：赵霞[1] 梁婷婷[2] 裴强[3] 王洪波[4] 范玉磊[2] 魏中秋[2] 冯莉[2] 孙影[2] 

机构地区：[1]河北联合大学冀唐学院医学实验中心,河北唐山063300 [2]河北联合大学基础医学院病理学系,河北唐山063000 [3]河北联合大学附属遵化市人民医院心内科,河北唐山064200 [4]河北联合大学附属遵化市人民医院外科,河北唐山064200

出　　处：《中国医药导报》2015年第21期18-20,25,共4页China Medical Herald

基　　金：河北省引进留学人员科技活动项目(D2012003028)

摘　　要：目的观察硫氧环蛋白过氧化物酶3(Prdx-3)在血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥大中的作用,并探讨其作用机制。方法体外培养心肌细胞(H9C2)随机分为对照组、AngⅡ组、AngⅡ+转染对照组和AngⅡ+Prdx-3转染组。脂质体转染法将Prdx-3表达质粒转染心肌细胞,Western blot法检测Prdx-3蛋白表达,Real-time PCR法检测脑钠素(BNP)m RNA表达,二氯荧光素二乙酸(DCFH-DA)检测活性氧(ROS)水平。结果 Prdx-3表达质粒转染心肌细胞后,Prdx-3蛋白表达值为(0.88±0.12),高于转染对照组(0.38±0.05),差异有统计学意义(P<0.05)。与对照组比较,AngⅡ组BNP m RNA[(1.00±0.00)比(1.72±0.29)]、ROS[(3473±81)比(4439±111)]及Prdx-3蛋白表达水平[(0.33±0.05)比(0.72±0.14)]均明显增加,差异均有统计学意义(均P<0.05)。AngⅡ+转染对照组和AngⅡ组的BNP m RNA[(1.72±0.29)比(1.94±0.34)]、ROS[(4439±111)比(4285±167)]及Prdx-3蛋白水平[(0.72±0.14)比(0.75±0.11)]比较,差异无统计学意义(P>0.05)。与AngⅡ组比较,AngⅡ+Prdx-3转染组BNP m RNA[(1.72±0.29)比(1.29±0.15)]和ROS水平[(4439±111)比(3648±254)]明显下降,但Prdx-3蛋白水平[(0.72±0.14)比(1.89±0.37)]显著增高,差异均有统计学意义(均P<0.05)。结论 AngⅡ可通过ROS诱导心肌细胞肥大,而Prdx-3通过降低ROS抑制AngⅡ的作用。Objective To study the effect of peroxiredoxin-3 （Prdx-3, a noval type of peroxidase） on Angiotensin Ⅱ （Ang Ⅱ）-induced eardiomyocytes hypertrophy and explore the precious mechanism. Methods Cultured cardiomyocytes （H9C2） were randomly divided into four groups： control group, Ang Ⅱ group, Ang Ⅱ ＋vehicle （plasmid without prdx-3 gene） group, Ang Ⅱ ＋Prdx-3 plasmid group. Prdx-3 was transfected into cardiomyoeytes using the liposome infection. Western blot was used to evaluate Prdx-3 expression in cardiomyocytes, while levels of brain natriuretic peptide （BNP） mRNA and reactive oxygen species （ROS） were measured by Real-time PCR and DCFH-DA. Results The expression of Prdx-3 protein in transfected cardiomyocytes （0.88±0.12） was significantly higher than vehicle （0.38±0.05, P 〈 0.05）. Compared with control group, expressions of BNP mRNA, ROS and Prdx-3 in Ang 11 group all increased [（1.00±0.00） vs （1.72±0.29）, （3473±81） vs （4439±111）, （0.33±0.05） vs （0.72±0.14）, P 〈 0.05]. The difference of expressions of BNP mRNA [（1.72±0.29） vs （1.94±0.34）], ROS [（4439±111） vs （4285±167）] and erdx-3[（0.72±0.14） vs （0.75±0.11）] between Ang Ⅱ and Ang Ⅱ ＋vehicle groups were not statistically significant （P 〉 0.05）. Compared with Ang Ⅱ, expressions of BNP mRNA and ROS in Ang Ⅱ ＋Prdx-3 plasmid group were lower [（1.72±0.29） vs （1.29±0.15）, （4439±111） vs （3648± 254）, P 〈 0.05], while Prdx-3 level was further higher [（0.72±0.14） vs （1.89±0.37）, P 〈 0.05]. Conclusion AngH in- duced cardiomyocytes to generate ROS, which contributes to cell hypertrophy; however, Prdx-3 over-expression inhibits these ehanees by deereasing ROS level.

关 键 词：硫氧环蛋白过氧化物酶3 活性氧 心肌肥大 血管紧张素Ⅱ 

分 类 号：R542.2[医药卫生—心血管疾病]