肿瘤坏死因子-α在干酪乳杆菌细胞壁萃取物诱导的川崎病冠状动脉炎小鼠模型中的作用  被引量:4

THE ROLE OF TNF-A IN A MURINE MODEL OF KAWASAKI DISEASE ARTERITIS UNDUCED WITH A LACTOBACILLUS CASEI CELL WALLL EXTRACTS

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作  者:朝鲁门其其格 刘潇婷[2] 杨光路[1] 

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.

关 键 词:动脉炎 动脉炎模型 干酪乳杆菌 川崎病 肿瘤坏死因子-Α 

分 类 号:R725.4[医药卫生—儿科]

 

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