摘要
目的:探讨家兔慢性心力衰竭(心衰)时心肌细胞核、肌浆网钙离子/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)蛋白表达及活性的改变。方法:16只家兔随机分为两组,假手术组、心衰组各8只,通过超容量负荷联合压力负荷建立家兔心衰模型,于术后7周观察左心室结构、血液动力学的变化及心肌细胞核、肌浆网CaMKⅡ的表达和活性的改变。结果:与假手术组比较,心衰组左心室重量指数[(132±0.06)g/kg vs(3.61±0.09)g/kg]、左心室舒张末压[(-1.50±0.50)mmHg vs(23.00±2.37)mmHg(1 mmHg=0.133 kPa)]显著升高(P均<0.05),左心室短轴缩短率(37.83%±3.58%vs 17.38%±3.13%)及左心室射血分数(71.92%±4.56%vs 38.50%±6.07%)明显降低(P均<0.05);心衰组心肌细胞核和肌浆网的CaMKⅡ蛋白表达及活性均显著高于假手术组(P均<0.05)。结论:心肌细胞核及肌浆网CaMKⅡ蛋白表达及活性增加可能是心衰发生的机制之一。
Objective： To explore the changes of protein expression and activity of calcium/calmodulin-dependent protein kinase-Ⅱ （CaMK-Ⅱ） in myocardium nucleus and sarcoplasmic reticulum in experimental rabbits with heart failure （HF）. Methods： A total of 16 rabbits were divided into 2 groups： Sham group and HF group, the HF model was established by volume overload plus pressure overload, n=8 in each group and all animals were treated for 7 weeks. Left ventricular structure, hemodynamic parameters and protein expression and activity of CaMK-II in myocardium nucleus and sarcoplasmic reticulum were examined and compared between 2 groups. Results： Compared with Sham group, HF group presented increased left ventricular mass index （LVMI） （1.32 ± 0.06） g/kg vs （3.61 ± 0.09） g/kg, LVEDP （-1.50 ± 0.50） mmHg vs （23.00 ± 2.37） mmHg, all P〈0.05; while decreased left ventricular shorten fraction （37.83 ± 3.58） % vs （17.38 ± 3.13） % and LVEF （71.92 ± 4.56） % vs （38.50 a： 6.07） %, all P〈0.05. The protein expression and activity of CaMK-II were both higher in HF group than Sham group, all P〈0.05. Conclusion： Increased protein expression and activity of CaMK-Ⅱ in myocardium nucleus and sarcoplasmic reticulum might be one of the mechanisms for HF occurrence in experimental rabbits.
出处
《中国循环杂志》
CSCD
北大核心
2015年第10期1000-1003,共4页
Chinese Circulation Journal
