摘要
目的研究肠道微生态对三硝基苯磺酸(trinitro-benzen-sulfonic acid,TNBS)诱导大鼠结肠炎肠黏膜上皮细胞紧密连接蛋白的保护作用。方法建立TNBS诱导大鼠结肠炎模型。实验分为正常组、模型组和双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)组。进行疾病活动指数(DAI)和组织学损伤评分,用ELISA法测定结肠组织TNF-α、IL-10和血清内毒素水平,采用免疫组织化学染色检测紧密连接(tight junction,TJ)相关蛋白occludin的分布。结果TNBS诱导大鼠结肠炎后,DAI和组织学损伤评分增高,结肠组织TNF-α水平升高,IL-10水平降低和血清内毒水平升高,而经双歧杆菌嗜酸乳杆菌肠球菌三联活菌处理后,DAI和组织学损伤评分有明显下降,结肠组织TNF-α水平降低,IL-10水平升高和血清内毒素水平降低,组间比较差异有显著性(P<0.05)。TNBS诱导大鼠结肠炎后,TJ结构遭到破坏,TJ相关蛋白的表达亦减少,而双歧杆菌嗜酸乳杆菌肠球菌三联活菌(金双歧)处理后可使TNBS引起的TJ结构受损减轻,相关蛋白的表达增多(P<0.05)。结论肠道微生态对TNBS诱导大鼠结肠炎肠黏膜上皮细胞TJ蛋白具有明显的保护作用,其可能的机制是通过纠正肠道微生态,上调肠上皮细胞TJ蛋白occludin的表达,降低结肠组织TNF-α水平,提高IL-10水平,从而抑制内毒素通过紧密连接进入体循环。
Objective To investigate the effect of intestinal microecology protectiong tight junction proetein between the epithelial cells of intestinal mucosal barrier in rats with trinitro-benzen-sulfonic acid（TNBS） induced colitis.Methods Acute colitis was induced by giving TNBS.28 rats including male and female were randomized into normal group（n=8）,TNBS group（n=10） and live combined bifidobacterium and lactobacillus tables（golden bific） group（n=10）.Diarrhea and bloody stool as well as colonic histology were observed.The levels of tumor necrosis factor-α（TNF-α） and interleukin-10（IL-10） in colonic tissue and endotoxin in blood were determined with ELISA.The expression of occludin between the epithelial cells of intestinal mucosal barrier was detected by histochemical stain method.Results The inflammatory symptoms and histological damages of colonic mucosa in golden bifid group were better than those in TNBS group,but were worse than those in normal group.Compared with TNBS group,the levels of TNF-α and endotoxin in blood were significantly reduced（P0.05）;the level of IL-10 and the expression of occludin between the epithelial cells of intestinal mucosal barrier were remarkably elevated（P0.05）.Conclusion The data suggests that intestinal microecology has the ability of protecting tight junction protein between the epithelial cells of intestinal mucosal barrier through the mechanism of activating occludin protein,increasing the production of IL-10 and reducing the level of TNF-α and endotoxin in blood.
出处
《临床消化病杂志》
2010年第1期21-24,共4页
Chinese Journal of Clinical Gastroenterology
