核转录因子-kB在急性心肌梗死血管内皮细胞损伤中的作用  

Role of nuclear factor-kB in endothelial injury in acute myocardial infarction

作　　者：廖新学[1] 李欣[2] 马中富[3] 王礼春[1] 杜志民[1] 董吁刚[1] 马虹[1] 

机构地区：[1]中山大学附属第一医院心内科,广东广州510080 [2]中山大学附属第一医院急诊科,广东广州510080 [3]中山大学附属第一医院普内科,广东广州510080

出　　处：《中国危重病急救医学》2008年第7期413-415,共3页Chinese Critical Care Medicine

基　　金：广东省科技计划基金资助项目（2004830601016,2006836004010）;广东省自然科学基金资助项目（5001676）

摘　　要：目的观察急性心肌梗死（AMI）再灌注后核转录因子-kB（NF—kB）活性和血清肿瘤坏死因-a（TNF—a）、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—kB活性，放射免疫法测定TNF—a含量，酶联免疫吸附试验测量sTM水平。结果NF—kB活性以及TNF—a和sTM水平在溶栓后0．5h就明显升高，1h达高峰，3、12和24h逐渐下降；各时间点的数值均显著高于对照组（P均〈0．05）；1h时的各数值均显著高于24h（P均〈0．05）。sTM与NF—kB活性和TNF—a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—kB活化、TNF—a增加和内皮细胞损伤；NFxB活化可能是造成血管内皮细胞损伤的重要机制之一。Objective To examine the change in nuclear factor-kB （NF-xB） activity, tumor necrosis factor-a （TNF-a） 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-kB 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-~B activity, TNF-a 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-kB activity and the levels of TNF-a and sTM （all P〈0.05）. Conclusion These results indicate that NF-kB is activated and the levels of TNF-a and sTM rise significantly after reperfusion in AMI. The activation of NF-kB maybe one of the most important pathogenic mechanism of endothelial injury.

关 键 词：血管内皮细胞 核转录因子-KB 心肌梗死 急性 

分 类 号：R542.22[医药卫生—心血管疾病]