目的 研究心脏能量代谢脂肪酸β氧化过程中关键脱氢酶之一的短链脂酰辅酶A脱氢酶(short-chain acly-coen-zyme A dehydrogenase,SCAD)与心肌肥大之间的关系,探索治疗心血管疾病的新靶点.方法 利用自发性高血压大鼠(spontaneous hypertension rats,SHR)和异丙肾上腺素皮下注射两种心肌肥大动物模型,以及苯肾上腺素(PE)刺激的心肌细胞肥大模型,检测SCAD在蛋白水平和mRNA水平上表达量的改变;并采用siRNA对SCAD进行干扰,观察对肥大分子指标的影响.结果 以上动物模型和细胞模型中SCAD的蛋白表达水平都有明显的下降,mRNA水平表达量也有一定程度的下降.针对SCAD的siRNA干扰后可导致心肌细胞SCAD的表达明显下降,而肥大标记因子ANF、BNP的表达明显上调,进一步明确了SCAD与心肌细胞肥大的关系.结论 心肌肥大时SCAD的蛋白水平和mRNA水平均明显下降,干扰SCAD后心肌细胞肥大指标上升,说明SCAD的下降可能参与心肌肥大的病理过程,上调SCAD有可能成为干预心肌肥大的重要环节之一.%Aim In cardiac energy metabolism, fatty acids β-oxidation is one of the most important step, and short-chain acly-coenzyme A dehydrogenase ( SCAD ) is a key enzyme in this process. The aim of this study is to investigate the relationship between SCAD and myocardial hypertrophy. Methods Spontaneous hypertension rats and isoproterenol stimulated model were used as in vivo models, and phenyleph-rine -stimulated cardiomyocyte were used as in vitro model, the protein expression of SCAD was measured by western blot analysis and mRNA expression of SCAD was evaluated by real-time PCR method. Results Protein and mRNA expression of SCAD decreased both in vivo and in vitro. The SCAD specific siRNA inhibited the expression of SCAD, which also increased the expression of hypertrophy-related genes including atrial natriuretic factor( ANF ) and brain na-triuretic peptide( BNP ) in cultured cardiocytes. Conclusion In myocardial hypertrophy model, the expression of protein and mRNA of SCAD declines significantly, and specific siRNA inhibits the expression of SCAD, ANF and BNP increase, which means that SCAD may play an important role in myocardial hypertrophy. To raise the expression of SCAD could become an important part in intervening cardiac hypertrophy.
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