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目的:研究在压力负荷下辛伐他汀对钙调神经磷酸酶介导的心肌肥大的影响。方法:选用SD大鼠随机分为3组:假手术组(n=10)、单纯模型组(n=10)和辛伐他汀组(n=10)。大鼠通过腹主动脉缩窄建立压力超负荷模型,8周后测定左室重量指数,B超检测左室形态结构,Westernblot检测心肌CaN蛋白表达,RT-PCR法检测心肌CaNmRNA水平。结果:①单纯模型组和辛伐他汀组心肌肥厚指数明显高于假手术组,辛伐他汀组心肌肥厚指数明显低于单纯模型组(P<0.05)。②单纯模型组和辛伐他汀组心肌CaN蛋白及CaNmRNS表达水平高于假手术组(P<0.05),辛伐他汀组低于单纯模型组(P<0.05)。结论:辛伐他汀可能参与干预钙调神经磷酸酶介导的通路从而抑制心肌肥厚的形成。
AIM: To investigate the effect of simvastatin on calcineurin-mediated cardiac hypertrophy under pressure overload. Methods: SD rats were randomly divided into 3 groups: sham operation group (n = 10), simple model group (n = 10) and simvastatin group (n = 10). The pressure overload model was established by abdominal aorta constriction in rats. The left ventricular mass index was measured after 8 weeks, the morphology of left ventricle was detected by B ultrasound, CaN protein expression was detected by Western blot and CaN mRNA level by RT-PCR. Results: ① The indexes of cardiac hypertrophy in simple model group and simvastatin group were significantly higher than those in sham-operation group and simvastatin group (P <0.05). ② The levels of CaN protein and CaNmRNS in myocardium in simvastatin group and simvastatin group were significantly higher than those in sham operation group and simvastatin group (P <0.05). Conclusion: Simvastatin may be involved in the intervention of calcineurin-mediated pathway to inhibit the formation of cardiac hypertrophy.