风湿性心脏病心房颤动的左心房中calpain-I的表达和意义

Expression and significance of calpain-I in left atria of patients with rheumatic heart disease

目的:检测calpain-I在风湿性心脏病心房颤动(Af)患者左心房中的表达,研究其在Af发病机制中的作用。方法:选择接受外科换瓣手术的风湿性心脏病患者43例,其中窦性心律(RSR)组15例,阵发性Af(PAf)组8例,慢性Af(CAf)组20例。在外科手术中取左心房组织,应用免疫印迹方法测定calpain-I和肌钙蛋白I(cTnI)的蛋白含量。用逆转录-聚合酶链反应法测定calpain-I在 mRNA水平上的表达。结果:①与RSR组比较,CAf组calpain-I蛋白含量增加到(344±101.9)%(P<0.01);cTnI的蛋白含量则降低到(45.0±13.4)%(P<0.01)。②CAf组calpain-I的mRNA表达为2.49±0.86,比PAf组的(1.23±0.31)和RSR组(0.89±0.23)的明显增加(均P<0.01);calpain-I的蛋白含量与cTnI的蛋白含量也呈明显负相关(r=-0.898,P<0.01)。而PAf组calpain-I和cTnI蛋白表达则无明显变化。③CAf组calpain-I的蛋白含量和mRAN水平的表达分别与左心房内径和Af持续时间呈明显正相关(P<0.05或P<0.01)。结论:CAf时左心房组织calpain-I的蛋白含量明显升高,促进心房结构和功能的改变,参与Af的发病机制。

Objective：To detect the expression of calpain-I at the left atria of patients with rheumatic heart disease（RHD）, and to investigate the role of the calpain-I on the mechanism of atrial fibrillation（Af）. Method：Fortythree patients with RPID who required valve-replacement were included. There were 15 patients with regular sinus rhythm（group RSR）, 8 patients with paroxysmal Af（group PAf） and 20 patients with chronic Af（group CAf）. Western blotting was used to examine the content of calpain-I and troponin-I. RT-PCR was used to detect mRNA expression of calpain-I. Result： Compared with Group RSR, the contents of calpain-I of group CAr increased to （344±101.9） % （P〈0.01） ,and the expression of calpain-I in mRNA level reached at 2.49±0. 86,which was significantly higher than that of Group RSR （0.89±0.23） and PAf（1. 23±0.31） （P〈0. 001）. The contents of troponin-I decreased to （45.0 ± 13.4）% （P〈0. 001 ）. There was a negative relationship between the protein content of calpain-I and troponin-I. There were no change in expression of the above two proteins in group PAf. In group CAf, the protein content and mRNA level of calpain-I were positively relative to left atrial dimension and Af duration respectively（all P value〈0.05）. Conclusion： The expression of Calpain-I increases in leftchronic fibrillating atria of patients with rheumatic heart disease and might contribute to the pathogenesy of Af.