【摘要】 目的探讨同时激活PPARα、PPAR s激活剂对血管紧张素Ⅱ(AngⅡ)诱导肥大心肌细胞的影响。方法体外原代培养新生大鼠心肌细胞,分别以不同浓度非诺贝特(PPARα激活剂)和或吡格列酮(PPARγ激活剂)预处理24 h后,加用AngⅡ刺激诱导肥大心肌细胞模型。采用软件分析细胞表面积,以MTT比色法测定心肌细胞活力,用RT-PCR法检测α-MHC和胚胎基因β-MHC mRNA的表达。结果与对照组相比,非诺贝特、吡格列酮显著逆转了AngⅡ诱导的心肌细胞肥大,抑制AngⅡ引起细胞活力改变,增加α-MHC mRNA表达,降低β-MHC mRNA的表达,α/-βMHC mRNA比值明显增加;相对两药处理组,上述指标与两药合用组无显著差异(P>0.05)。结论PPAR s信号通路激活能有效预防心肌细胞肥大,PPARαγ配体合用未见明显叠加效应。更多还原

【Abstract】 Objective To investigate the inhibitory effects of the ligands of peroxisome proliferator-activated receptors(PPARs),fenofibrate(PPARα activator) and pioglitazone(PPARγ activator)on the angiotensin Ⅱ(Ang Ⅱ)-induced cardiac hypertrophy in vitro.Methods A model of hypertrophy of neonatal rat cardiac myocytes was established with AngII stimulation.With the aid of Leca Qwin Image software,the surface area of cardiac myocytes was analyzed.The mRNA expression of α-MHC,β-MHC was measured by reverse transcription-polymerase chain reaction(RTPCR) and the cultured myocyte viability was estimated by MTT assay.Results Fenofibrate or pioglitazone pretreatment 24 h prior to AngⅡ stimulation,significantly reduced the cardiac hypertrophy(P<0.01-0.05),increased the expression of α/β-MHC mRNA,and inhibited the effect of Ang II on the cardiac myocyte viability in a dose-dependent manner.There were no significant differences in the above mentioned indices between fenofibrate and pioglitazone group.Conclusion Activating PPARs-dependent pathway prevents the cardiac hypertrophy,and there is no obvious additive effect when the 2 drugs are used in combination.更多还原