Model group were given trinitrobenzene sulfonic acid (TNBS) to coloclysis (50% TNBS, 0.25 ml / 100 mg), and the control group with saline, and then continued to raise 4 weeks. Using ELISA method to detect the serum level of IL-4, immunohistochemical method to detect the expression level of IL-4R, the expression level of the c-kit and TMEM16A in colon, Western blot method to detect the expression level of c-kit and TMEM16A protein. Results: (1), the serum
expression level of IL-4 detected by ELISA: the model group serum level of IL-4 was significantly higher than the control group (p < 0.05). (2), the results to immunohistochemical method: (1) the expression of IL-4R: the PI-IBS group significantly higher than the control group (p < 0.05); (2) the expression of the c-kit: the number of c-kit marking positive cells in model group was Alvelestat more than the control group (p < 0.05); (3) TMEM16A: the expression level of TMEM16A in model group was lower than the control group (p < 0.05). (3), the expression level of the c-kit and TMEM16A detected by Western blot: the results were consistent with the immunohistochemistry:
in model group c-kit marking positive cells were higher than control group (p < 0.05) and in model group, the expression level of TMEM16A waslower than the control group (p < 0.05) Conclusion: The expression level of IL-4 and IL-4R were significantly increased in PI-IBS model group; The ICC were injured by inflammation in PI – IBS model; Baricitinib The expression level of TMEM16A in model group was decreased; In PI-IBS Proteasome inhibitor drugs model, IL-4 could induce a higher expression level of TMEM16A, however the inflammation injury of ICCs can cause the decrease of TMEM16A expression, and what’s more, this phenomenon influence the readjustment of CaCCs, in turn, affects the ICC’s slow wave activity, and then ultimately affect the normal dynamic activities of the gut, and appear the clinical symptoms of PI-IBS.
Key Word(s): 1. PI-IBS; 2. TMEM16A; 3. ICC; 4. IL-4; Presenting Author: YUNZHI ZHAO Additional Authors: HE-SHENG LUO, FA-CAN ZHANG Corresponding Author: YUNZHI ZHAO Affiliations: Wuhan University; Guangxi Zhuang Autonomous Region Objective: To determine of the number and degree of activation of rectosigmoid junction mucosal mast cells (MC) in patients with diarrhea-predominant irritable bowel syndrome (IBS-D), and to explore the role of intestinal mucosal MC activation and tryptase in pathogenesis of IBS-D. Methods: 20 patients with IBS-D fulfilling the Rome III diagnostic criteria and and 10 healthy volunteers included in the study. One mucosa tissue was collected from the rectosigmoid junction mucosa during electronic colonoscopy, pathological examination to exclude the pathological changes such as colonic mucosa inflammation, tumor and so on. MC in colonic mucosa were stained by Immunohistochemistry.