【摘要】 目的:探讨分泌型卷曲相关蛋白5（s FRP5）在心肌细胞肥大中的表达情况及其发挥的作用。方法:体外培养SD乳鼠心肌细胞,应用血管紧张素Ⅱ（AngⅡ）诱导心肌细胞肥大。替米沙坦、PD123319分别阻滞血管紧张素1型受体（AT1R）、血管紧张素2型受体（AT2R）的表达,逆转录聚合酶链反应（RT-PCR）及蛋白免疫印迹法（Western bolt）检测sFRP5、脑利钠肽（BNP）及肿瘤坏死因子-a（TNF-a）的表达。结果:s FRP5能够在心肌细胞中表达。sFRP5 mRNA及蛋白水平、BNP蛋白水平的表达随AngⅡ干预时间的延长而增加,48 h达到最高值（P<0.05）。与AngⅡ(10^-6 mol/L)组相比,AngⅡ+替米沙坦（10μmol/L）组sFRP5 mRNA和蛋白水平显著降低（P<0.05）,AngⅡ+PD123319（10μmol/L）组sFRP5 mRNA和蛋白水平差异无统计学意义（P>0.05）;与AngⅡ(10^-6 mo1/L)+sFRP5（0 ng/ml）组比较,AngⅡ(10^-6 mo1/L)+sFRP5（10 ng/ml）组及AngⅡ(10^-6 mo1/L)+sFRP5（100 ng/ml）组BNP蛋白及TNF-a的蛋白表达水平明显下降（P<0.05）。结论:在AngⅡ诱导的心肌细胞肥大过程中,主要通过血管紧张素Ⅱ型受体上调sFRP5的表达,且sFRP5在抑制心肌细胞肥大中发挥作用。更多还原

【Abstract】 Objective: To investigate the expression and effect of secreted frizzled-related protein 5（sFRP5） in rat’s cardiomyocyte hypertrophy in vitro.Methods: Neonatal rat’s ventricular myocytes were cultured in vitro, cardiomyocyte hypertrophy was induced by Ang Ⅱ. Telmisartan and PD123319 were used to block angiotensin type 1 receptor（AT1R） and angiotensin type 2 receptor（AT2R） respectively. RT-PCR and Western-blot analysis were conducted to examine the expressions of sFRP5, BNP and TNF-α.Results: sFRP5 was expressed in cardiomyocytes. The mRNA and protein expressions of sFRP5, protein expression of BNP were increased by prolonged time of Ang Ⅱ treatment, the maximum expression was observed at 48 h, P <0.05. Compared with Ang Ⅱ(10^-6 mol/L) group, the mRNA and protein expressions of sFRP5 in Ang Ⅱ +Telmisartan（10 μmol/L） group were decreased, P<0.05, those expressions were similar in Ang Ⅱ +PD123319（10 μmol/L） group, P>0.05. Compared with Ang Ⅱ(10^-6 mol/L)+sFRP5（0 ng/ml） group, protein expressions of BNP and TNF-α were decreased in Ang Ⅱ(10^-6 mol/L)+sFRP5（10 ng/ml） group and in Ang Ⅱ(10^-6 mol/L)+sFRP5（100 ng/ml） group respectively, P<0.05.Conclusion: For in vitro process of Ang Ⅱ induced neonatal rat’s cardiomyocyte hypertrophy, using Ang Ⅱ receptor could up-regulate sFRP5 expression and sFRP5 plays an important role in cardiomyocyte hypertrophy.更多还原