短链酰基辅酶A脱氢酶在大鼠生理性和病理性心肌肥大中的作用

 目的：研究短链酰基辅酶A脱氢酶(short-chain acyl-CoA dehydrogenase, SCAD)在大鼠生理性和病理性心肌肥大中的变化，探讨其与心肌肥大之间的关系。方法：以自发性高血压大鼠作为病理性心肌肥大模型，游泳运动训练性大鼠作为生理性心肌肥大模型。检测大鼠的血压、左室重量指数、血清和心肌游离脂肪酸含量、SCAD mRNA、蛋白表达及其酶活性的变化，采用超声心动图观察心脏的结构及功能。结果：与对照组比较，运动组大鼠出现了明显的离心性肥大，心肌收缩功能增强；而高血压组大鼠呈现出明显的向心性肥大，心肌收缩功能减退。与对照组比较，运动组和高血压组大鼠的左室重量指数均明显增高，但两组间比较无显著差异，二者发生了相同程度的心肌肥大。与对照组比较，运动组大鼠左心室SCAD mRNA和蛋白表达均明显上调，酶活性增高，血清和心肌游离脂肪酸含量明显减少；而自发性高血压大鼠左心室SCAD mRNA和蛋白表达均明显下调，酶活性下降，血清和心肌游离脂肪酸含量明显增多。结论：SCAD在生理性和病理性心肌肥大中呈现出不一致的变化趋势，可能作为区别2种不同心肌肥大的分子标志物以及病理性心肌肥大的潜在治疗靶点。

Effect of short-chain acyl-CoA dehydrogenase on cardiac hypertrophy induced by hypertension or exercise training

AIM: To investigate the differential expression of short-chain acyl-CoA dehydrogenase (SCAD) in cardiac hypertrophy induced by hypertension or exercise training. METHODS: Spontaneously hypertensive rats (SHR) were used as the model of pathological cardiac hypertrophy. The swim-trained rats were used as the model of physiological cardiac hypertrophy. The systolic pressure, cardiac hypertrophy parameters, echocardiogram parameters, free fatty acid in serum and cardiac muscle, and the expression and activity of SCAD in the left ventricle were measured. RESULTS: Compared with the control rats, trained rats developed an athletic heart, of which cardiac function was enhanced, whereas SHR developed hypertensive cardiac hypertrophy, of which cardiac function was deteriorated. Compared with the control rats, the ratios of left ventricular weight to body weight were both increased in trained rats and SHR, showing that the degrees of cardiac hypertrophy were similar in the 2 models. Compared with the control rats, the decrease of free fatty acid both in serum and myocardium indicated that the fatty acid utilization was increased in the left ventricle of trained rats. Meanwhile, the expression and activity of SCAD in the left ventricle of trained rats were increased. However, free fatty acid both in serum and myocardium were increased, indicating that the fatty acid utilization was decreased in the left ventricle of SHR. Furthermore, SHR had the decreased expression and activity of SCAD in the left ventricle. CONCLUSION: The changes of SCAD are different in cardiac hypertrophy induced by hypertension and exercise training, indicating that SCAD may be used as a molecular marker of physiological and pathological cardiac hypertrophy, and a potential therapeutic target of pathological cardiac hypertrophy.