Expression of intestinal mucosa tight junctions claudin proteins and mRNA in patients with irritable bowel syndrome

Objective：To investigate the changes of intestinal mucosa tight junctions （TJs） claudin-1, -3, -4 proteins and mRNA changes in patients with irritable bowel syndrome （IBS） and to elucidate their possible roles in the changes of bowel evacuation habit and formation. Methods： Claudin-1, -3, -4 proteins and mRNA were evaluated in intestinal mucosa in control group, D-IBS （diarrhea IBS） group and C-IBS （constipation IBS） group with immunohistochemical assay and Realtime-PCR. Results： It was observed that claudin-1, -3, -4 proteins were localized in the membranes of epithelial cells along the entire length of the plasma membrane including the apical end of the epithelial cells. The elaudins were concentrated at the site of TJs only. Claudin-1, 3, -4 mRNA and claudin-1 protein in small intestinal mucosa and colonal mucous in D-IBS group were significantly downregulated （P〈0.05）. Claudin-1, -3, -4 mRNA and proteins in small intestinal mucosa and colonal mucous in C-IBS group were significantly upregulated （P〈0. 05）. There was no significant difference in the expression of claudin-3 protein in both small intestinal mueosa and colonal mucous between D-IBS group and control group（P〉0.05）. Similarly, no significantly different expression of claudin-4 protein in colonal mucous in D-IBS group was found compared with control group （P〉0.05）. Otherwise, the expression of claudin 4 protein in small intestinal mucosa decreased in D-IBS group （P〈0.05）. Conclusion： Claudin-1, -3, -4 may play a potential important role in the changes of bowel evacuation habit and formation in patients with IBS. It is not due to the localization changes of claudin proteins in TJ, but may be caused by the quantitative changes of the expression of TJ proteins and mRNA.

Proteomic analysis of down-regulated proteins in colonic mucosa of chronic slow transit constipation rats

Objective： To investigate the alternations of proteins in the colonic mucosa of chronic slow transit constipation （STC） rats with a 2-DE-based proteomic method and analyze the function of these down-regulated proteins so as to provide theoretical basis for the pathogenesis of intestinal mucosa of chronic STC rats. Methods： STC model was established by feeding rats with 8 mg/（kg＇d） diphenoxylate for 120 d. An experimental model of chronic STC rat was used for separation of proteomics from colonic mucosa using two-dimensional electrophoresis （2-DE）. Proteins altered in expressional level were identified by Image Master 2DElite, mass spectrometry, and bibliometrics were applied to identify the differential protein expression and their clinical s observed in the pathogenesis lgn of ificance and function were analyzed. Results： Obvious differential protein expression was STC, including mast cell protease （A1）, non-specific dipeptidase （A2） and chondrosome succinate dehydrogenase precursor （A3）. The expressions of A1, A2 and A3 were down-regulated in the gel graph of STC rats Conclusion： The down-regulation of chondrosome succinate dehydrogenase, mast cell protease as well as non-specific dipeptidase in rat colon suggests the functional impairment of the oxidoreduction of mitochondrion is very important in the genesis and development of STC. The immunological reaction of STC rats is weakened, and the function of digesting and absorbing protein may be damaged to some extent.

高血糖素样肽-2对大鼠失血性休克复苏后肠道免疫功能的影响

目的 研究高血糖素样肽 2 (Glucagon likepeptide 2 ,GLP 2 )对大鼠失血性休克复苏后胆汁中分泌型IgA (sIgA)、肠黏膜蛋白质和DNA含量的影响。方法 采用大鼠经股动脉放血及自体血回输的方法复制休克复苏模型 ,连续腹腔注射GLP 2 ,7d后收集大鼠胆汁测定sIgA、采集门静脉血测定血内毒素及制备小肠黏膜标本测定小肠黏膜蛋白质和DNA含量。结果 休克复苏组胆汁中sIgA仅为对照组的 78%左右 ,而GLP 2组与对照组接近 ;小肠黏膜蛋白质和DNA含量GLP 2组显著高于休克复苏组 ,门静脉血内毒素也显著减少。结论 GLP 2能够改善大鼠休克复苏后肠道免疫功能 。