| Background: Inflammatory bowel disease(IBD), which include two kinds of disease,Crohn’s disease(CD)and Ulcerative Colitis(UC),is a chronic non—specific intestinal inflammatory disease. Its pathogens has not yet been fully clarified.And It is always hard to cure and diagnose. What’s more, the existence of many disadvantages on its curing for example the long treatment cycle, the serious side effects and the ease of relapse made some patients with bad efficacy of ethnodrugs turn to surgery for help. With the lucubrating of microecologics in recent years, Probiotics have been applied to the adjuvant therapy of IBD patients and gained some certain effects.Objective: Discuss the role of Saccharomyces boulardii in immunoregulation of intestinal mucosa through its application to the mice that was infected by inflammatory bowel disease.Method: 2,4,6-Trinitrobenzene Sulfonic Acid was adopted to induce the mice IBD model. 50 clean grade mice of half male and half female in weight of 18-22 grams, age of 6-8 weeks were divided into 5 groups: normal control group(Group A), pathologic control group(Group B), Mesalazine treating group(Group C), Saccharomyces boulardii treating group(Group D) and Saccharomyces boulardii combined Mesalazine treating group(Group E). 10 mice were contained in each group. All mice were fasted but not water-deprived for 24 hours. The four groups were dealed with isopyknic mixed liquid of 100mg/kg 5%TNBS(m/v) and absolute ethyl alcohol. The enema tube was pulled out after pulsed injection. The mice’s anus was quietly clamped and picked up the tails to head down for about 1 minute for the sake of promoting fully contact of molding pharmaceutical s and colonic mucous. Group A was clystered by the same amount of normal saline. Normal raising was followed and then A and B were gavaged by normal saline. The rest were treated by corresponding medicine.Observing the general condition, weight changing, stool property and bloody stool level of mice everyday was proceeded and then killed mice 7 days later. Intestinal tissues were collected. Some of them were observed of pathological changes by microscope with colon tissue paraffin section after HE dying. Others were homogenated and determined the expression of Interleukin-10 and interferon-γ in intestinal tissue by Enzyme Linked Immunosorbent Assay(ELISA).Result: 1.9 mice were died after modeling and remodeling was adopted immediately for supplementary. The mice died during treating was not refilled again and the data was not contained Mice of group A were in normal activities but the rest group were in slowness reaction. The fur was loose. The food-intake was reduced. And the weight was declined. With the processing of treating, the symptoms of mice in group C, D and E were improved. DAI of group B was 3.33±0.528, tissue damage overall grade was 4.11±0.78, histologic grade was 9.44±1.62 and IFN-γ content of intestinal tissue was 62.41±7.96pg/ml, which were higher than the other groups. On the contrary, IL-10 content of intestinal tissue was 62.41±7.96pg/ml, which was higher than the others. The differences were statistically significant.(p<0.01). 3. Group C and D made no significant differences in every detection indexes and no statistical significance existed(P>0.05). 4. DAI of group E was 0.70±0.399, tissue damage overall grade was 1.10±0.57, histologic grade was 2.50±1.08 and IFN-γ content of intestinal tissue was 194.23±16.45pg/ml which was lower than group B, C and D. IL-10 content of intestinal tissue was 100.84±4.305pg/ml, which was higher than group B, C and D.And differences made statistical significance(P<0.01).Conclusion: 1.The induced inflammatory bowel disease model by TNBS was successful generally. The modeling time was short and operation was easy. 2.Both Saccharomyces boulardii and Mesalazine were treating-effective and no visible difference was observed in treating effect. 3.The result of Saccharomyces boulardii combined Mesalazine group was better than them alone. 4. Saccharomyces boulardii was supposed to be inflammation controllable because of its adjustment of intestinal immune function,and then the symptom were improved. |
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