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目的 探讨白介素8(rhIL-8)参与兔心肌缺血/再灌注损伤的机制,为减轻再灌注损伤探索新的治疗途径。方法 结扎兔冠状动脉左前降支(left anterior descending coronary artery,LAD)造成缺血1小时,再灌注3.5小时。实验分两组:缺血/再灌注组(MI/R,n=8)和假结扎组(Sham MI/R,n=8)。结果 MI/R组发生严重的心肌损伤,包括受累心肌髓过氧化物酶(myeloperoxidase,MPO)活性增大和血清肌酸磷酸激酶-MB同工酶(CPK-MB)、异构前列腺素(eoi-PGF_(2α))水平增高(均P<0.01)。血清IL-8浓度逐渐升高,免疫组化示受损心肌区血管内皮基底膜呈IL-8阳性染色。结论 血管内皮细胞释放的IL-8是吸引中性粒细胞浸润于缺血区心肌,造成缺血/再灌注损伤的因素之一。
Objective To investigate the mechanism of interleukin-8 (rhIL-8) involved in myocardial ischemia / reperfusion injury in rabbits and to explore a new therapeutic approach to reduce reperfusion injury. Methods Ligation of left anterior descending coronary artery (LAD) in rabbits caused ischemia for 1 hour and reperfusion for 3.5 hours. The experiment was divided into two groups: ischemia / reperfusion group (MI / R, n = 8) and sham group (Sham MI / R, n = 8). Results Severe myocardial injury occurred in MI / R group, including increased myocardial myeloperoxidase (MPO) activity, serum creatine phosphokinase-MB isoenzyme (CPK-MB), eo-prostaglandin PGF 2α) (all P <0.01). Serum IL-8 concentration gradually increased, immunohistochemistry showed myocardial injury area of vascular endothelial base membrane IL-8 positive staining. Conclusion The release of IL-8 by vascular endothelial cells is one of the factors that induce neutrophil infiltration into the ischemic myocardium and cause ischemia / reperfusion injury.