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．

R 725．4

 收稿日期: 2017－01－18;修回日期: 2017－02－18
基金项目: 内蒙古科技厅科技计划项目(2014)
作者简介: 朝鲁门其其格(1973－)，女，内蒙古医科大学附属医院儿科主任医师。