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目的 :了解压力负荷性肥厚心肌过氧化物酶体活化受体α(PPARα)和中链脂酰基辅酶A脱氢酶(MCAD)mRNA的表达变化 ,探讨PPARα对肥厚心肌脂肪酸 β氧化关键酶基因表达的调控作用及肥厚心肌能量底物的变化。方法 :观察大鼠腹主动脉缩窄术后 1、4、8、16周血流动力学参数、心室重塑指标、血清和心肌游离脂肪酸 (FFA)的含量及PPARα和MCADmRNA的表达变化。结果 :随着肥厚程度的增加 ,血清和心肌FFA蓄积增加 ,心肌PPARα和MCADmRNA的表达也逐渐下调 ,且与脂肪酸的利用下调相一致。结论 :肥厚心肌PPARα活性下调 ,与MCAD基因表达变化一致 ;PPARα在转录水平调控脂肪酸氧化酶基因的表达 ;PPARα与肥厚心肌能量底物转换密切相关
OBJECTIVE: To investigate the changes of PPARα and MCAD mRNA expression in hypertrophic myocardium of hypertensive myocardium and to investigate the effect of PPARα on the expression of the key enzyme gene of fatty acid β-oxidation in hypertrophic myocardium Regulation and change of hypertrophic myocardium energy substrate. Methods: The changes of hemodynamics, ventricular remodeling, serum and myocardial free fatty acids (FFA) and the expression of PPARα and MCAD mRNA were observed at 1, 4, 8 and 16 weeks after abdominal aortic constriction in rats. RESULTS: With the increase of hypertrophy, the accumulation of FFA in serum and myocardium increased, the expression of myocardial PPARα and MCAD mRNA also gradually decreased, which was consistent with the down-regulation of fatty acid utilization. CONCLUSION: PPARα activity is down-regulated in hypertrophic myocardium, which is consistent with the change of MCAD gene expression. PPARα regulates the expression of fatty acid oxidase gene at transcriptional level. PPARα is closely related to energy substrate conversion in hypertrophic myocardium