CAJ | 학술논문

目的观察急性心肌梗死(AMI)再灌注后核转录因子-κB(NF-κB)活性和血清肿瘤坏死因-α(TNF-α)、可溶性血栓调节蛋白(STM)水平的动态变化,探讨心肌缺血/再灌注对内皮细胞损伤的作用及机制.方法随机选取进行静脉溶栓再通的AMI患者(AMI再灌注组,8例),并以健康体检者8例作为正常对照组.以电泳迁移率变动分析法(EMSA)检测NF-κB活性,放射免疫法测定TNF-α含量,酶联免疫吸附试验测量sTM水平.结果 NF-κB活性以及TNF-α和sTM水平在溶栓后0.5 h就明显升高,1 h达高峰,3、12和24 h逐渐下降;各时间点的数值均显著高于对照组(P均＜0.05);1 h时的各数值均显著高于24 h(P均＜0.05).sTM与NF-κB活性和TNF-α之间的动态变化有明显相关性(P均＜0.05).结论 AMI再灌注后存在着NF-κB活化、TNF-α增加和内皮细胞损伤;NF-κB活化可能是造成血管内皮细胞损伤的重要机制之一.
목적 관찰급성심기경사(AMI)재관주후핵전록인자-κB(NF-κB)활성화혈청종류배사인-α(TNF-α)、가용성혈전조절단백(STM)수평적동태변화,탐토심기결혈/재관주대내피세포손상적작용급궤제.방법 수궤선취진행정맥용전재통적AMI환자(AMI재관주조,8례),병이건강체검자8례작위정상대조조.이전영천이솔변동분석법(EMSA)검측NF-κB활성,방사면역법측정TNF-α함량,매련면역흡부시험측량sTM수평.결과 NF-κB활성이급TNF-α화sTM수평재용전후0.5 h취명현승고,1 h체고봉,3、12화24 h축점하강;각시간점적수치균현저고우대조조(P균＜0.05);1 h시적각수치균현저고우24 h(P균＜0.05).sTM여NF-κB활성화TNF-α지간적동태변화유명현상관성(P균＜0.05).결론 AMI재관주후존재착NF-κB활화、TNF-α증가화내피세포손상;NF-κB활화가능시조성혈관내피세포손상적중요궤제지일.
Objective To examine the change in nuclear factor-κB (NF-κB) activity, tumor necrosis factor-α (TNF-α) and soluble thrombomodulin (STM) levels at different time following reperfusion in acute myocardial infarction (AMI), and to identify the role of ischemia/reperfusion after ischemia in injury to endothelial cells and its relevant mechanism. Methods AMI group included 8 randomly selected patients with AMI, and a normal control group (n= 8) compoising individuals who underwent health check. NF-κB activity in monocytes was determined by electrophoretic mobility shift assays (EMSA). The level of TNF-a was measured by radio-immunity and sTM was measured by enzyme linked immunosorbent assay (ELISA).Results The NF-κB activity, TNF-α and sTM levels raised dramatically at 0.5 hour after reperfusion,reaching peak at 1 hour and declined gradually at 3, 12 and 24 hours. The levels of all the determined parameters at every time point were significantly higher than that of normal control group, and their levels at 1 hour were significantly higher than that at 24 hours (all P＜0.05). There was a positive correlation between the NF-κB activity and the levels of TNF-α and sTM (all P＜0.05). Conclusion These results indicate that NF-κB is activated and the levels of TNF-α and sTM rise significantly after reperfusion in AMI.The activation of NF-κB maybe one of the most important pathogenic mechanism of endothelial injury.