摘要
目的探讨阿托伐他汀(atorvastatin)对血管紧张素Ⅱ(AngⅡ)诱导的肥大心肌细胞的抑制作用及对转录因子FoxO1表达的影响。方法将H9C2细胞分为3组,对照组:未给予任何干预;心肌肥大组:给予AngⅡ(10-7 mol/L)刺激细胞;阿托伐他汀组:预先给予atorvastatin(10-5 mol/L),30min后AngⅡ(10-7 mol/L)刺激细胞。western-blotand real time PCR检测H9C2细胞FoxO1蛋白及mRNA含量,脑钠肽(brain natriuretic pepide,BNP)作为判断心肌肥大的指标。结果 AngⅡ诱导心肌细胞肥大后FoxO1表达较正常心肌细胞明显降低(P<0.05),而给予阿托伐他汀干预的肥大心肌细胞其FoxO1表达较肥大心肌明显升高(P<0.05)。结论阿托伐他汀可能通过上调FoxO1表达,从而抑制心肌肥大。
Objective To assess effects of atorvastatin（Ator） on cardiac myocyte hypertrophy induced by angiotensin Ⅱ（Ang Ⅱ） and transcription factor FoxO1 expression for theoretical bases of preventing and treating myocardial hypertrophy.Methods H9C2 cells were divided into 3 groups：normal control;hypertrophic group：cells were stimulated by AngⅡ（10-7 mol/L）;ator group：cells were treated with ator（10-5 mol/L）,30 min before adding AngⅡ（10-7 mol/L）.The method of western-blot and real time PCR were adopted to evaluate the FoxO1 expression.Brain natriuretic pepide（BNP） was the symbol of cardiac myocyte hypertrophy.Results The mRNA and protein level of FoxO1 were significantly decreased in the hypertrophic group as compared with normal control and atorvastatin group.Conclusion Atorvastatin inhibits cardiac myocyte hypertrophy and upregulates the expression of FoxO1.
出处
《西部医学》
2012年第3期453-455,共3页
Medical Journal of West China
