容量超负荷大鼠左室内向整流钾通道蛋白表达的研究

摘要

Objective To observe the protein expression of inward rectifier potassium channel (IK1) in the left ventricle of volume-overload heart failure (HF) rats. Methods Volume-overload heart failure model was created in rats by abdominal arteriovenous fistula method. Meanwhile, control rats were sham-operated (SO). Electrocardiographic variables, plasma brain natriuretic peptide (BNP) level, and ratio of heart weight and body weight (HW/BW) were measured 8 weeks later to evaluate the heart function. The protein expression of IK1 isoforms in the left ventricle was evaluated by immunohistochemistry and Western blot. Results The HF rats showed significant decline in systolic and diastolic heart functions (P<0.01) as well as significant increase in BNP level and HW/BW (P<0.01). In adult rat left ventricles, Kir2.1, Kir2.2 and Kir2.3 were all expressed in the cell membrane and cytoplasm. The protein expression of IKl isoforms above decreased significantly in failing heart compared with SO heart by 13.2%, 24.7% and 8.9%, respectively (P<0.01). Conclusion The protein expression of IK1 isoforms in the left ventricle of volume-overload rats is significantly decreased.%目的 观察容量超负荷心衰大鼠左室心肌内向整流钾通道(IK1)各亚型的蛋白表达.方法 通过腹主动脉-下腔静脉造瘘法建立容量超负荷大鼠心衰模型,同时设立假手术组.术后8周后用心动超声、血清脑钠肽(BNP)、心体比等评价心衰模型,采用免疫荧光染色和Western blot测定两组大鼠左室心肌IK1的亚型Kir2.1、Kir2.2、Kir2.3的蛋白表达.结果 心衰组与假手术组大鼠相比,心动超声示心脏收缩与舒张功能均明显减低(P＜0.01),血清BNP水平明显升高(P＜0.01),心体比明显增大(P＜0.01),IK1通道的亚型Kir2.1、Kir2.2、Kir2.3在细胞膜与细胞质均表达,其蛋白表达量均明显下降(P＜0.01),分别下降了13.2％00、24.7％、8.9％.结论 慢性心力衰竭大鼠左室心肌Iκ1通道各亚型的蛋白表达量均明显降低.