摘要目的 研究葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎小鼠肠黏膜屏障功能受损情况及其机制.方法 建立DSS诱导的慢性溃疡性结肠炎小鼠模型,设置正常对照组和DSS组,完全随机分组,每组25只,监测小鼠的体质量及结肠长度变化;结肠组织病理检查确认造模成功并评估结肠黏膜屏障的完整性;通过伊文思蓝在肠内的通透性分析评估小鼠结肠黏膜屏障的功能;免疫荧光染色和Western印迹评估肠黏膜屏障完整性相关蛋白的表达情况.结果 与正常对照组小鼠相比较,DSS组小鼠的体质量较低[(25.6±0.7)g比(23.5 ±0.7)g,t=2.14,P＜0.05],结肠长度较短[(7.3±0.4)cm比(5.6±0.2)cm,t=3.975,P＜0.001];结肠组织病理结果显示肠黏膜变薄,部分区域肠黏膜缺损;结肠肠腔内滴入的伊文思蓝进入肠黏膜的量较多,波长620 nm的光密度(0D620)/结肠组织重量(g)较高[(0.1l±0.01)比(0.15±0.01),t=4.174,P＜0.05];免疫荧光及Western印迹结果显示结肠黏膜中ZO-1、Claudin-1、F-肌动蛋白的表达减少.结论 DSS诱导的慢性溃疡性结肠炎小鼠的肠黏膜屏障结构及功能均受损.

abstractsObjective To study the damage and mechanism of intestinal mucosal barrier function in mice with ulcerative colitis induced by Dextran sulphate sodium (DSS).Methods Mice models of chronic ulcerative colitis induced by DSS were established.The mice were completely randomized into normal control group and DSS group,25 mice in each group.The body weight and colon length of the mice were monitored.The pathological examination of colon tissue was confirmed the success of the model and assessed the integrity of the colonic mucosal barrier;Evan's Blue's intestinal permeability analysis assessed the function of colon mucosal barrier;immunofluorescence staining and Western blot were used to evaluate the expression of intestinal mucosal barrier integrity-related proteins.Results Compared with the normal control group,the DSS group had lower body weight [(25.6 ± 0.7) g vs (23.5 ± 0.7) g,t =2.14,P ＜ 0.05],and the colon length was shorter [(7.3 ± 0.4) cm vs (5.6 ± 0.2) cm,t =3.975,P ＜ 0.001];colonic pathological results showed that the intestinal mucosa became thinner and part of the intestinal mucosa was defective;Evan's Blue instilled into the intestinal lumen was more abundant into the intestinal mucosa,and the optical density at 620 nm (OD620)/colon tissue weight (g) was higher [(0.11 ± 0.01) vs (0.15 ± 0.01),t =4.174,P ＜ 0.05];immunofluorescence and Western blot results showed lower expression of ZO-1,Claudin-1,and F-actin in colonic mucosa.Conclusion The structure and function of intestinal mucosal barrier in DSS-induced chronic ulcerative colitis mice is impaired.