神经调节蛋白1对心肌梗死急性期大鼠心肌组织钾、钙离子通道蛋白表达的影响

Effects of Neuregulin 1 on myocardium potassium and calcium channels expression in acute myocardial infarction rats

目的探讨神经调节蛋白1(NRG-1)对心肌梗死急性期大鼠心肌组织钾、钙离子通道蛋白表达的影响。方法45只健康SD大鼠随机分为3组,假手术组(SO组)、急性心肌梗死模型组(AMI组)、急性心肌梗死rhNRG-1干预组(NRG-1组),每组15只。建立急性心肌梗死模型24 h后取心脏梗死周边区心肌组织,以Western blot法检测瞬时外向钾通道KV1.4和L型钙通道β亚单位LTCCsβ的蛋白表达情况。结果 AMI组和NRG-1组模型建立成功,心肌梗死面积比较差异无统计学意义[(35.4±3.6)%vs.(33.3±4.9)%,P>0.05]。与SO组比较,AMI组KV1.4降低(0.43±0.23 vs.0.20±0.17,P<0.05);而LTCCsβ差异无统计学意义(1.05±0.31 vs.1.00±0.21,P>0.05)。与AMI组相比,NRG-1组(0.66±0.29)梗死周边区心肌组织KV1.4蛋白表达显著增加,LTCCsβ蛋白表达(0.18±0.11)显著下降,差异均有统计学意义(t=20.95,P<0.05)。结论心肌梗死急性期给予NRG-1干预,能够上调KV1.4,下调LTCCsβ的蛋白表达,可发挥稳定心电保护心肌的作用。

Objective To investigate the effects of neural regulatory protein 1 （ NRG-1） on acute myocardial infarc-tion rats myocardium potassium , calcium ion channel protein expression .Methods Forty-five healthy SD rats were randomly divided into 3 groups , the sham operation group （ SO group ） , acute myocardial infarction model group （ AMI group ） , acute myocardial infarction rhNRG-1 intervention group （NRG-1 group）, and 15 rats in each group.Establish acute myocardial in-farction model, after 24 h, took peri-infarcted myocardium and used Western blot to detect transient outward potassium chan -nel KV1.4 and L type calcium channel beta subunit ltccs beta protein expression .Results AMI group and NRG-1 group’ model was successfully established .Myocardial infarction area did not show statistical significance [（33.3 ±4.9）% vs. （35.4 ±3.6）%, P 〉0.05].Compared with the SD group, AMI group’s KV1.4 reduced （0.43 ±0.23 vs.0.20 ±0.17, P 〈0.05）;and the differences of LTCCs beta showed no statistical significance （1.05 ±0.31 vs.1.00 ±0.21）.Compared with AMI group, NRG-1 group （0.66 ±0.29） peri-infarcted area of myocardium ’ s KV1.4 protein expression increased sig-nificantly, LTCCs beta protein expression （0.18 ±0.11） decreased significantly , the differences were statistically significant （ t =20.95, P 〈0.05）.Conclusion It demonstrated that the NRG-1 for acute myocardial infarction can increase KV 1.4, reduce the protein expression of LTCCs beta , which can play a role in the stability of ECG of myocardial protection .