摘要
目的观察壳寡糖(chitosan oligosaccharide,COS)对2,4,6一三硝基苯磺酸(2,4,6-trinitrobenzene sulfonic acid,TNBS)/乙醇法诱导的小鼠溃疡性结肠炎(ulcerative colitis,UC)的改善作用,探讨其治疗UC的作用机制.方法采用TNBS/乙醇法制备UC小鼠模型,小鼠随机分3组:正常组、模型组、COS组.造模成功后给予干预治疗,分别在12、24 h处死全部小鼠,进行一般状态、形态及组织学观察(肉眼观察、显微镜观察);应用Western blot检测COS组小鼠于COS处理0、12、24 h后对核因子-kB(nuclear factor-kB,NF-kB)表达的影响.结果 COS组小鼠一般状态较模型组好转.模型组小鼠结肠黏膜组织损伤肉眼观积分较正常组明显增高(12 h组:4.5±0.5 vs 0;24 h组:4.67±0.47 vs 0),差异有统计学意义(P<0.05).COS组肉眼积分较模型组明显下降(12 h组:2.67±0.47 vs 4.5±0.5;24 h组:1.83±0.69 vs 4.67±0.47),差异有统计学意义(P<0.05).COS 12 h组肉眼积分较24 h组差异不显著(2.67±0.47 vs 1.83±0.69),无统计学意义(P>0.05).模型组小鼠结肠黏膜组织病理积分较正常组明显升高(12 h组:8.00±0.63 vs 0;24 h组:8.17±0.75 vs 0),差异有统计学意义(P<0.05).COS组小鼠结肠组织病理积分较模型组明显下降(12 h组:3.67±0.52 vs 8.00±0.63;24 h组:3.83±0.41 vs8.17±0.75),差异有统计学意义(P<0.05).COS 12 h组小鼠结肠组织病理积分与COS24 h组比较差异不显著(3.67±0.52 vs 3.83±0.41),无统计学意义(P>0.05).COS组小鼠于COS处理12、24 h后NF-kB表达下调,表明COS抑制NF-kB表达.结论 COS通过抑制NF-冔B的表达对TNBS/乙醇法诱导的UC小鼠有改善作用.
AIM To observe the anti-inflammatory effect of chitosan oligosaccharide （COS） in mice with experimental ulcerative colitis （UC） and to explore the underlying mechanism. METHODS A mouse model of UC was established by 2,4,6-trinitrobenzene sulfonic acid （TNBS）/ ethanol enema. Mice were randomly divided into three groups： a normal group, a model group, and a COS group. After treatment, the general state, the gross morphology score, and the pathology score were compared among the three groups. RESULTS The general state of mice in the COS group was better than that of the model group. The gross morphology score for colon mucosal injury significantly increased in the model group compared with the normal group （12 h： 4.5± 0.5 vs 0; 24 h： 4.67 ± 0.47 vs 0; P 〈 0.05）. The gross morphology score for colon mucosal injury declined significantly in the COS group compared with the model group （12 h： 2.67 ± 0.47 vs 4.5± 0.5; 24 h： 1.83 ± 0.69 vs 4.67 ± 0.47; P 〈 0.05）. There was no significant difference in the gross morphology score for colon mucosal injury between 12 h and 24 h in the COS group （2.67 ± 0.47 vs 1.83 ± 0.69, P 〉 0.05）. The pathology score increased significantly in the model group compared with the normal group （12 h： 8.00 ± 0.63 vs 0; 24 h： 8.17 ± 0.75vs 0; P 〈 0.05）. The pathology score declined significantly in the COS group compared with the model group （12 h： 3.67 ± 0.52 vs 8.00 ± 0.63; 24 h： 3.83 ± 0.41 vs 8.17± 0.75; P 〈 0.05）. There was no significant difference in the pathology score between 12 h and 24 h in the COS group （3.67 ± 0.52 vs 3.83 ± 0.41, P 〉 0.05）. After treatment with COS, the expression of nuclear factor-κB （NF-κB） declined significantly, suggesting that COS can inhibit the expression of NF-κB. CONCLUSION COS may exert anti-inflammatory effect on TNBS-induced UC in mice by inhibiting the expression of NF-κB.
出处
《世界华人消化杂志》
CAS
2017年第15期1352-1359,共8页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No.81202399/H3001~~
关键词
溃疡性结肠炎
壳寡糖
核因子-KB
Ulcerative colitis
Chitosan oligo-saccharide
Nuclear factor-κB
