溃疡性结肠炎小鼠肠道通透性改变与TNF-α及NF-κB P65的关系

Changes of colonic permeability and its correlation with TNF-α,NF-κB p65 in ulceration colitis mice

目的:采用2.5%葡聚糖硫酸钠(DSS)定量灌胃诱导小鼠溃疡性结肠炎(UC),观察小鼠结肠通透性改变与肿瘤坏死因子α(TNF-α)及NF-κB p65的关系。方法:48只ICR小鼠随机分为2组(n=24):对照组和模型组。模型组小鼠给予2.5%DSS定量灌胃诱发小鼠急性UC,对照组小鼠予同体积的蒸馏水灌胃代替。记录两组小鼠疾病活动指数(DAI),9 d后测定两组小鼠结肠组织病理学评分、结肠通透性、TNF-α及NF-κB p65。统计分析DAI、结肠通透性、TNF-α与NF-κB p65之间的相关性。结果:与对照组比较,模型组小鼠DAI、结肠病理学评分、结肠通透性、TNF-α、NF-κB p65均显著增高(P均<0.01)。小鼠DAI增高与结肠通透性密切相关(P均<0.01),结肠通透性增高与TNF-α、NF-κB p65密切相关(P均<0.01)。结论:与对照组小鼠相比,DSS造模小鼠的结肠通透性显著增高,并与TNF-α、NF-κB p65增高呈正相关。TNF-α、NF-κB p65增高导致结肠通透性增高,进而导致炎症免疫反应过度增强,可能是UC发病的重要环节。

Objective： To study the changes of colonic permeability and its correlation with TNF-α, NF-κB p65 in indextran sulphate sodium （DSS） induced ulcerative colitis（UC） of mice. Methods： Forty-eight ICR mice were randomly divided into the control group and the model group. The acute UC model was induced by quantified intragastric administration of 2.5 % DSS in mice. The disease activity index （DAI）, histopathology scores, colonic permeability, expression of TNF-α, NF-κB 1065 in colonic tissue were determined. The change of colonic permeability and its correlation with DAI, TNF-α, NF-κB 1365 were analyzed. Results： Compareded with the control group, DAI colonic permeability of colonic tissue, and the expression of TNF-α NF-κB p65 in the model group were increased significantly （ P 〈 0.01, P 〈 0.01 ）. The increased colonic permeability correlated with DAI （P 〈 0. 01 ）, and the expression of TNF-α（ P 〈 0.01 ）, NF-κB p65 （P 〈 0.01 ）changed significantly. Conclusion： The alteration of colonic permeability and increased expression of TNF-α, NF-κB p65 may play important roles in the occurrence and development of UC.