【摘要】 目的以大鼠胚胎来源的心肌细胞为模型,观察氟伐他汀对心肌细胞凋亡的调控作用,并探讨其可能机制。方法通过MTT检测法检测细胞活性,用流式细胞仪检测细胞凋亡,用实时定量PCR以及Western Blot方法检测转化生长因子β1(TGF-β1)及其受体的表达。结果氟伐他汀能够以浓度依赖性的方式降低H9c2细胞的活性,10μM氟伐他汀处理H9c2细胞后其凋亡率增加,处理4 d后H9c2细胞凋亡率为54.9%;氟伐他汀能够上调TβRⅡmRNA和蛋白的表达,而对TGF-β1及TβRⅠ的表达无明显的上调作用。结论氟伐他汀能够诱导H9c2细胞的凋亡,这种凋亡诱导作用可能与氟伐他汀对TβRⅡ的上调作用有关。更多还原

【Abstract】 Objective To study the regulation of apoptosis of cardiomyocytes by Fluvastatin and its mechanism based on the cell model of rat embryo-myocardial cells.Methods The cell viability was observed by MTT assay,and the cell apoptosis was examined by flow cytometry.The expression of TGF-β1 and its receptor were examined by real time RT-PCR and western blot.Results Fluvastatin could reduce the viability of the H9c2 cells by concentration-dependent method.Treatment of H9c2 cells with 10 μM fluvastatin could induce the apoptosis of the cells,and 4 days after treatment with 10 μM fluvastatin,the apoptosis rate of H9c2 cells reached 54.9%.Fluvastatin could up regulate the expression of TβRⅡ mRNA and protein but could not significantly up regulate the expression of TGF-β1 or TβRⅠ.Conclusion Fluvastatin can induce the apoptosis of H9c2 cells and this induction may relate to the up-regulation of TβRⅡ.更多还原