摘要
目的:探讨非诺贝特(fenofibrate)对血管紧张素Ⅱ(AngⅡ)诱导的肥大心肌细胞的抑制作用及对FoxO1表达的影响。方法:首先采用AngⅡ诱导心肌细胞肥大,将细胞分为三组:对照组:未给予任何干预;心肌细胞肥大组:AngⅡ(10-7mol/L)刺激细胞;治疗组:先给予fenofibrate(10-5mol/L),30min后AngⅡ(10-7mol/L)刺激细胞。应用蛋白免疫印迹法(western-blotting)和实时定量PCR法(real time PCR)检测各组细胞中转录因子FoxO1的蛋白质及mRNA含量,心肌细胞肥大的判断使用脑钠肽(brain natriuret icpepide BNP)。结果:心肌细胞肥大组的FoxO1表达较对照组明显降低,而治疗组的FoxO1表达较心肌肥大组明显升高。结论:非诺贝特可能通过上调FoxO1表达,从而抑制心肌细胞肥大。
Objective： To investigate effect of fenofibrateon on myocardial 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： nomal control group;hypertrophy group： cells were stimulated by AngⅡ（10-7 mol/L）;treatment group：cells were treated with fenofibrate（10-5 mol/L）,30 min before adding AngⅡ（10-7 mol/L）.The method of western-blotting and real time PCR were adopted to detect the FoxO1 expression.Brain natriuretic pepide（BNP） was the symbol of cardiac myocyte hypertrophy.Results： The mRNA and protein level of FoxO1 decreased significantly in the hypertrophy group compared with that in the normal control and treatment group.Conclusion： Fenofibrate inhibits cardiac myocyte hypertrophy,upregulates the expression of FoxO1.
出处
《现代生物医学进展》
CAS
2012年第8期1449-1451,1429,共4页
Progress in Modern Biomedicine
