中文摘要：

目的 探讨抗巨噬细胞移动抑制因子单抗（抗MIF单抗）对小鼠急性溃疡性结肠炎（UC）发病的干预作用及其可能调控机制。方法 以葡聚糖硫酸钠（DSS）诱导制备小鼠急性UC模型,小鼠分为正常组、UC模型组、抗MIF单抗干预组和生理盐水组。造模及药物干预期间观察小鼠一般情况并行疾病活动指数（DAI）评分,7d后断颈处死全部小鼠,行结肠大体损伤评分,HE染色后光镜下观察结肠病理改变,免疫组化染色观察巨噬细胞移动抑制因子（MIF）、肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）等促炎因子在结肠组织炎症细胞的表达情况,实时荧光定量PCR（real-timePCR）检测结肠组织核因子-κβ（NF-κβ）p65mRNA的表达水平。结果 与正常组相比,其余三组小鼠结肠炎症病变明显,MIF、TNF-α、IL-6等促炎因子的表达水平明显升高（P〈0.05）;与模型组相比,干预组结肠黏膜损伤程度减轻,抗MIF单抗显著改善MIF、TNF-α、IL-6等促炎因子的表达水平（P〈0.05）,而生理盐水组与其差异无统计学意义（P〉0.05）。real-timePCR结果显示应用抗MIF单抗的小鼠能显著抑制结肠组织NF-κβp65mRNA的表达水平。结论 抗MIF单抗对小鼠UC的发病有明显的干预作用,可能通过抑制NF-κβ信号通路,减少促炎因子的表达发挥作用。

英文摘要：

Objective To investigate the protective effect and possible regulatory mechanism of anti-macrophage migration inhibitory factor monoclonal antibody （anti-MIF Ab）on acute ulcerative colitis （UC） in mice. Methods Acute ulcerative colitis model in mice was established by dextran sulfate sodium （DSS）, to observe the protective effect of anti-MIF Ab on ulcerative eolotis in mice. The experiment was divided into normal group, UC model group, anti-MIF Ab intervention group and saline group. During modeling and the period of administration, to ob- serve general situations and score Disease Activity Index （DAI） of mice, after 7 days, all mice were killed, per- forming the gross damage score in colon, observing the colonic histopathological changes under the light microscope on HE staining, viewing the expression conditions of serum inflammatory cytokins such as MIF,TNF-α, IL-6 in in- testinal inflammatory cells on immunohistochemieal staining, using real-time quantitative （real-time PCR） to ana- lyze the expression levels of NF-Kβ p65 mRNA in colon tissue. Results Compared with the normal group, the de- grees of colonic inflammation were significantly severe in the other three groups, the expression levels of serum in- flammatory cytokines such as MIF,TNF-α, IL-6 were remarkably increased （ P 〈 0. 05 ） ; compared with the model group, the degrees of colonic mucosa damage were alleviated in intervention group. Anti-MIF Ab could obviously improve the expression levels of serum inflammatory cytokines such as MIF, TNF-α, IL-6 （P 〈 0.05 ） , but no sig- nificant differences between saline group and model group. The results of real-time PCR showed that mice using an- ti-MIF Ab could apparently inhibit the expression level of NF-Kβ p65 mRNA. Conclusion Anti-MIF Ab has a strongly protective effect against ulcerative colitis in mice, maybe the inhibition of NF-Kβ signal pathway and the decreasion of inflammatory eytokines play a central factor resulting from this conclusion.