乳酸杆菌对溃疡性结肠炎大鼠肠黏膜Toll样受体2及核因子-kappa B表达的影响

Effect of lactobacillus on the expression of Toll-like receptor 2 and NF-κB in the colonic mucosa of rats with experimental ulcerative colitis

目的：观察乳酸杆菌对溃疡性结肠炎大鼠肠黏膜Toll样受体2（TLR2）及核因子-kappa B（NF-κB）表达的影响,探讨乳酸杆菌辅助治疗溃疡性结肠炎的机制.方法：采用三硝基苯磺酸/乙醇法诱导大鼠溃疡性结肠炎模型.观察并评估大鼠一般状态及组织损伤情况,以RT-PCR法和免疫组织化学分别检测TLR2、NF-κB表达.结果：乳酸杆菌组组织损伤情况明显较模型组减轻.模型组大鼠肠黏膜TLR2、NF-κB表达情况明显高于正常对照组和乳酸杆菌组.结论：乳酸杆菌可以通过抑制TLRs/NF-κB通路发挥对溃疡性结肠炎的辅助治疗作用.

Objective： To study the effect of lactobacillus on the expression of Toll-like receptor 2 （TLR2） and NF-κB in colonic mucosa of rats with 2,4,6-trinitrobenzenesulfonic acid and 50% alcohol（1 ： 1, V/V）-induced ulcerative colitis （UC）. Methods： Sixty healthy male SD rats were randomly divided into normal control group （N）, model group （M） and lactobacillus group. UC models were set up in group M and group L. Then the rats in group L were given lactobacillus solution by oral garages for three weeks. The disease activity index and histopathological score were observed. The expressions of TLR2 and NF-~cB were detected by RT-PCR and immunohistochemistry. Results： DAI and histopathologieal score in group L were slighter than those of the model group. The expression of TLR2 and NF-κB in the model group increased significantly than those of group N and group L. Conclusion： The TLRs/NF-κB pathway may be involved in the pathogenesis of UC. Lactobacillus can reduce the inflammation in the colonic mucosa of rats with experimental ulcerative colitis by inhibiting the expression of TLR2 and NF-κB.