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机构地区:[1]内蒙古医科大学附属医院儿科,内蒙古呼和浩特010050 [2]内蒙古医科大学
出 处:《内蒙古医科大学学报》2017年第3期211-214,共4页Journal of Inner Mongolia Medical University
基 金:内蒙古科技厅科技计划项目(2014)
摘 要:目的:现有研究已有证据表明包含肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)在内的多种细胞因子在川崎病的致病机制中起到作用。但迄今为止,我们尚未明确TNF-α在川崎病动脉炎进程中起到什么样的作用,本研究旨在从组织病理学角度来证实抗TNF-α在治疗动脉炎中的作用以及TNF-α在小鼠川崎病模型动脉炎的发生中所起到的作用。方法:利用英夫利昔单抗作为TNF-α阻断药物治疗干酪乳杆菌诱导的川崎病小鼠模型。观察其器官组织病理改变以及血管炎的发生率、损害及炎症程度。结果:实验组小鼠血浆TNF-α于诱导后1d开始显著升高(P<0.05),血管炎发生率为80%,表现包括血管壁增厚,弹性纤维紊乱断裂,大量炎性细胞浸润;阻断组小鼠血浆TNF-α无明显升高,血管炎发生率为20%,空白对照组未见血管炎。结论:基于组织病理学的观察,得出TNF-α对于川崎病动脉炎的发生起到重要作用。Objective:There is evidence that existing studies of various cytokines,including tumor necrosis factor-α(TNF-α),play a key role in pathogenesis of Kawasaki disease.However,we have not yet clear TNF-α plays what role in Kawasaki disease arteritis process.Therefore,this study aimed to verify from the perspective of histopathological effect of anti-TNF-α in the treatment of arterial inflammation in arthritis and TNF-α in mouse models of Kawasaki disease occurs in the arteries role.Methods:Using a mouse model of Kawasaki disease induced Lactobacillus casei and infliximab as TNF-α blocker therapy.Observe the pathological changes of organs and tissues as well as the incidence of vascular inflammation.Results:The plasma TNF-α in the experimental group began to increase significantly at the 1st day after induction(P〈0.05),the incidence of vasculitis was 80%,showed that the blood vessel wall thickened,elastic fiber ruptured,and the infiltration of inflammatory cells;No significant increase in plasma TNF-α in the blockage group,the incidence of vasculitis was 20%;The control group has no vasculitis.Conclusion:Based on the observation of histopathology,derived TNF-α for the occurrence of Kawasaki disease arteritis play an important role.
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