【摘要】 目的通过检测Akt和FoxO1基因在大鼠超负荷性心肌肥大过程中的表达,探讨心肌肥大时的细胞周期调控机制。方法采用升主动脉缩窄的方法制作大鼠超负荷心肌肥大动物模型,通过三维彩色超声技术评价心肌肥大程度,采用RT-PCR技术检测心肌组织Akt和FoxO1的mRNA表达,用Westernblots方法检测Akt磷酸化水平。结果与假手术组相比,模型组的左室后壁厚度(LVPW)、室间隔厚度(IVS)增加(P<0.01),左室舒张末内径(LVDD)减小(P<0.01)。模型组心肌组织中FoxO1的mRNA表达下调(P<0.01),Akt的基因表达没有明显变化但蛋白的磷酸化水平显著增加(P<0.01)。结论大鼠超负荷性心肌肥大时Akt激活,同时FoxO1的表达下调。更多还原

【Abstract】 Objective To detect the expression of Akt and FoxO1 in cardiac muscle of rats with pressure overload cardiac hypertrophy to explore the regulation of cell cycle in hypertrophy.Methods The pressure overload cardiac hypertrophy modles(n = 10)were made by stenosis of the ascending aortic artery,10 rats were selected randomly as non stenosis sham control.Eight weeks after the operation,the left ventricular posterior wall(LVPW),interventricular septum thickness(IVS)and left ventricular end-diastolic(LVDD)of each rat were detected by echocardiogram.mRNA expression of Akt and Foxo1 was conducted by semiquantitative RT-PCR.Western blot was used to analysis the levels of phosphorylated Akt.Results The thickness of LVPW and IVS was significantly increased(P<0.01),and the internal diameter of LVDD was decreased in operated group(P<0.01)compared with sham.The expression of FoxO1 mRNA was downregulated(P<0.01)and the level of phosphorylated Akt was increased(P<0.01)in operated group compared with control,but without obvious difference for the mRNA level of Akt between two groups.Conclusion The activation of Akt and downregulation of FoxO1 might be involved in the mechanism of cardiac hypertrophy.更多还原