摘要
目的:探讨解耦联蛋白-2(UCP-2)与诱导型一氧化氮合酶(iNOS)在大鼠心肌缺血预适应(IPC)保护机制中的作用。方法:采取结扎左冠状动脉的方法复制大鼠心肌缺血-再灌注(I/R)模型。IPC组行3次缺血5 min、再灌注10 min的预处理,分别于预处理0、6、12、24和48 h后进行30 min缺血及120 min再灌注;对照组剖胸后不结扎左冠状动脉,分别采用Western blot及比色法检测心肌中UCP-2蛋白活性及iNOS活性。结果:IPC后各组UCP-2活性均增高(与I/R组比较,P<0.05),其中0 h组UCP-2表达水平最高(与I/R组比较,P<0.01),24 h组和48 h组心肌iNOS活性显著升高(与I/R组比较,P<0.05)。结论:UCP-2和iNOS共同参与了大鼠心肌缺血预适应的心肌保护作用。
Objective： To investigate the effect of uncoupling protein 2 （UCP-2） and inducible nitric oxide synthase （iNOS） in ischemic preconditioning （IPC） of the rat heart. Methods： The rat model of myocardial ischemia reperfusion （I/R） injury was established by ligation of the left coronary artery. The rats in both the I/R and IPC groups were subjected to 30 min of ischemia followed by 120 min of reperfusion after pre-conditioned for 0, 6, 12, 24 and 48 hours, and those of the IPC group underwent three episodes of 5 min ischemia coupled with 10 min reperfusion. The contents of UCP2 and iNOS in the myo cardium were determined. Results： Compared with the I/R group, the expressions of UCP-2 in the myocardium of the 0, 6, 12, 24 and 48 h IPC groups increased significantly（P 〈 0.05 ）, and so was the activity of iNOS in the 24 and 48 h IPC groups （P 〈 0. 05 ）. Conclusion ： Both UCP-2 and iNOS are involved in the protection of the rat myocardium during IPC.
出处
《医学研究生学报》
CAS
2007年第11期1159-1162,共4页
Journal of Medical Postgraduates
基金
南京军区"十一五"重点课题(批准号:Z-273)
