The Pathogenic Role Of MUC2 In Animal Models Of Inflammatory Bowel Disease

Background The incidence of Inflammatory bowel disease(IBD) is increased year by year, already is the world’s digestive systenm problems, an umbrella term that includes UC and CD, the exact etiology of the pathological is unclear, which may be related to intestinal flora and organization of immune-mediated mucosa injury related to the comprehensive effect of various factors, no single factor damage may trigger IBD。the destruction of the mucous membrane barrier also plays an important role, mucin MUC2 is composed of the main component of the intestinal mucosa,which is less research in China. Objective By observing the chronic colonic histological changes in IBD animal models, testing its CBir1, muc2 expression level, and giving different interventions to the model groups,we research muc2 in the role of IBD and understand evaluate the significance of the diagnosis for IBD,in order to investigate the pathogenesis of IBD. Methods Totally 60 SPE male BALb/c mice; which divided into 4 groups at random,each group consisting of 15 mice. ①normal control group: wild-type BAL / c mice no intervention,free drinking water.② TNBS+50% group: In zhe first day TNBS/50% ethanol 2.0mg/100μl was used,8 days with 50% TNBS/ethanol is 2.5 mg / 100 mu l enema, 15 th day with 50% TNBS/ethanol 3.0 mg / 100 mu l enema. ③Ketotifen + TNBS + 50% ethanol group: the steps of 50% TNBS/ethanol such as the second guoup, 0.5 mg Ketotifen which is soluble in 100 mu l physiological saline, and 30 min before every enema intraperitoneal injection in mice 100 mul the solution.(4) LPS + TNBS + OVA + 50% ethanol group: LPS(10 u g) and the OVA(20 u g) to join 100 mul 0.9 % in sodium chloride solution, respectively in four different time points(7,9,12,15) intraperitoneal injection of 100 mul, join the 100 mul with OVA(50(u g). 0. 9% sodium chloride solution, and intraperitoneal injection(18,19,20,21) in front of the enema. DAI was score for each group respectively, IN 9 day we kill one mice to PAS stain and the last one were put to death on day 22 Anti-CBir1 and MUC2 were detected in serum by ELISA)\. The colon tissues was used with HE and scored for HI. The expression of MUC2 and CBirl were mersured by immunohistochemistry and Periodic Acid-Schiff stain. Using SPSS 17.0 statistical software to process the experimental data, measurement data were expresser in mean±and standard deviation( x ±s), all the data of each group which were used single factor analysis of variance(ANOVA) to compare, analysis of variance of meaningful LSD- t test are compared, and two inspection level for alpha = 0.05, P < 0.05 can be expressed statistically significant. Results(1) Normal group: colonic mucosal epithelial cells were neat, did not see inflammatory cells invasion, TNBS + 50% alcohol, TNBS + 50% alcohol+TTF group and LPS + OVA + TNBS + 50%alcohol, group compared to normal group, plasma cells, lymphocytes, lymph follicles increased, while LPS + OVA + TNBS + 50% ethanol group of normal glandular structure basic disappearance, high levels of inflammation, even involving the intestinal wall layer.(2) The DAI score and HI score were higher than the normal group in TNBS,Ketotifen, LPS group, of which the differences had statistical significan(P<0.05). PAS stain MUC2 expression and immunohistochemical MUC2 expression,all of which in the TNBS+50% ethanol group were lower than in the TTF + TNBS +50% ethanol group, with statistical significance(P<0.05). The expression level of MUC2 in the TTF group was lower than in the LPS group, the differences was statistical significance(P<0.05). When compared with the normal control group, little statistical significance was found(P>0.05) between the saline group and the 50% ethanol group. When compared ketone group for PAS staining and immunohistochemical determination of MUC2 expression in the LPS group(P < 0.05), of which the differences had statistical significance(P<0.05). Conclusion(1) TNBS+50% ethanol were administrated via enema in BALb/c can be successfully copied as a model for IBD.(2) The MUC2 expression of BALb/c mouse model for IBD is lease,it may be related to IBD(3) TTF can activate mast cells to release induce intestinal inflammation.