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补体系统的活化与多种疾病的发病机制有关.无论在肾小球肾炎动物模型,抑或缺血/再灌注损伤心肌的标本中均有补体C_(1q),C_(3b),和C_(5b-9)的沉积及微血栓的形成,用来源于眼镜蛇毒的抗补体蛋白(cobra venom factor,CVF)预先耗竭补体可明显减轻损伤程度;在播散性血管内凝血(DIC)动物模型中,事先耗竭补体的动物血压下降幅度减小,血小板、纤维蛋白原、V因子和VⅡ因子等凝血因子的量无明显下降;在异种移植,超急性排斥反应(HAR)和血管排斥反应(AVR)在移植术后几分钟至几小时内发生,移植器官存在广泛的血管内凝血,在其血管内皮细胞上也有补体C_(5b-9)的沉积.鉴于内皮细胞在抗凝血中的作用,了解内皮细胞的功能及内皮细胞损伤的补体机制将有助于找到可能的防护措施.
The activation of the complement system is related to the pathogenesis of various diseases, including complement C_ (1q), C_ (3b), and C_ (5b) in both the animal model of glomerulonephritis and the myocardium with ischemia / reperfusion injury -9) and the formation of microthrombus. Pre-depletion of complement with cobra venom factor (CVF) derived from cobra venom significantly reduced the degree of injury. In disseminated intravascular coagulation (DIC) animal models, The decrease of blood pressure in animals that had depleted complement beforehand had no significant decrease in the amount of blood clotting factors such as platelet, fibrinogen, factor V and factor VII. In xenograft, hyperacute rejection (HAR) and vessel rejection (AVR) A few minutes to several hours after transplantation, there are extensive intravascular coagulation in transplanted organs and deposition of complement C 5b-9 on its vascular endothelial cells. Given the role of endothelial cells in anticoagulation, The function of cells and the complement mechanism of endothelial cell injury will help find possible protective measures.