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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 the inhibitory effect of fenofibrate on hypertrophic cardiomyocytes induced by angiotensin Ⅱ (AngⅡ) and its effect on FoxO1 expression. The cells were divided into three groups: control group: without any intervention; cardiomyocyte hypertrophy group: AngⅡ (10-7mol / L) stimulated cells; treatment group: fenofibrate (10- 5mol / L), 30min Ang Ⅱ (10-7mol / L) to stimulate cells. The protein and mRNA levels of transcription factor FoxO1 in each group were detected by western-blotting and real-time PCR. Brain natriuretic peptide (BNP) was used to judge the cardiomyocyte hypertrophy. Results: The FoxO1 expression in cardiomyocyte hypertrophy group was significantly lower than that in control group, while the expression of FoxO1 in treatment group was significantly higher than that in cardiac hypertrophy group. Conclusion: Fenofibrate may inhibit cardiomyocyte hypertrophy by up-regulating FoxO1 expression.