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抗巨噬细胞移动抑制因子单抗对结肠炎小鼠结肠NFκB、IκB表达的影响▲
Effect of antimacrophage migration inhibitory factor on NFκB、IκB Expression in mice with ulcerative colitis

微创医学 201712卷02期 页码:170-174

作者机构:1 桂林医学院研究生学院,广西桂林市541004;广西壮族自治区南溪山医院 2消化内科,3 病理科,桂林市541002

基金信息:▲基金项目:广西桂林市科学研究与技术开发计划项目(编号:科技攻关20140120-7-2);广西医疗卫生重点科研课题(编号:重2011018) *通信作者

DOI:DOI:10.11864/j.issn.1673.2017.02.04

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目的探讨抗巨噬细胞移动抑制因子单抗对结肠炎小鼠结肠NFκB p65、IκBα表达的影响。方法采用葡聚糖硫酸钠(DSS)诱导制备小鼠急性溃疡性结肠炎(UC)的模型,应用抗MIF单抗干预,观察抗MIF单抗对小鼠UC发病的干预作用。该实验分为正常对照组、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,第8天断颈处死全部小鼠,行结肠大体损伤评分,HE染色光镜下观察结肠病理改变,免疫组化染色观察NFκB p65、IκBα在结肠组织炎症细胞的表达情况。结果与正常组相比,UC模型组中NFκB p65的表达显著增加,而IκBα的表达稍增加,在抗MIF单抗治疗后,NFκB p65的水平明显低于UC模型组,并且IκBα含量增高。结论抗MIF单抗对DSS诱导的急性UC的小鼠具有保护作用,减低了小鼠结肠组织NFκB p65的表达水平,提高IκBα的表达水平,从而达到抑制UC小鼠结肠组织NFκB通路的过度激活的作用。
ObjectiveTo investigate the effect of antimacrophage migration inhibitory factor monoclonal antibody on NFκB p65、IκBα expression in mice with ulcerative colitis. MethodsAcute ulcerative colitis was induced by 5% dextran sulfate sodium(DSS). Then the protective effect of antiMIF Ab on ulcerative colotis in mice was observed. Forty mice were randomly distributed into normal control group, UC model group, antiMIF Ab intervention group and saline group.During modeling and the period of administration, to observe score Disease Activity and general situations Index(DAI) of mice, after 8 days killing all mice,performing the gross damage score in colon, observing the colonic histopathological changes under the light microscope on HE staining.The expression of NFκB p65、IκBα protein was detected by immunohistochemical staining. ResultsCompared with normal control mice, the level of NFκB p65 protein increased significantly in colon tissue of mice with UC,the level of IκBα slightly increased. After treatment with antiMIF Ab , the expression level of NFκB p65 significantly lower than that in UC model group,but the expression level of IκBα increased. ConclusionsThese findings suggest that antiMIF Ab had a protective effect on DSSinduced ulcerative colitis in mice downregulating NFκB p65 protein expression. Thus to inhibit the NFκB signaling pathway, excessive activation in the colon tissue of UC mice.

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