• Gut and Liver
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• v.12 no.6
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• pp.682-693
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• 2018

Background/Aims: Intestinal barrier dysfunction is a hallmark of inflammatory bowel diseases (IBDs) such as ulcerative colitis. This dysfunction is caused by increased permeability and the loss of tight junctions in intestinal epithelial cells. The aim of this study was to investigate whether estradiol treatment reduces colonic permeability, tight junction disruption, and inflammation in an azoxymethane (AOM)/dextran sodium sulfate (DSS) colon cancer mouse model. Methods: The effects of $17{\beta}$-estradiol (E2) were evaluated in ICR male mice 4 weeks after AOM/DSS treatment. Histological damage was scored by hematoxylin and eosin staining and the levels of the colonic mucosal cytokine myeloperoxidase (MPO) were assessed by enzyme-linked immunosorbent assay (ELISA). To evaluate the effects of E2 on intestinal permeability, tight junctions, and inflammation, we performed quantitative real-time polymerase chain reaction and Western blot analysis. Furthermore, the expression levels of mucin 2 (MUC2) and mucin 4 (MUC4) were measured as target genes for intestinal permeability, whereas zonula occludens 1 (ZO-1), occludin (OCLN), and claudin 4 (CLDN4) served as target genes for the tight junctions. Results: The colitis-mediated induced damage score and MPO activity were reduced by E2 treatment (p<0.05). In addition, the mRNA expression levels of intestinal barrier-related molecules (i.e., MUC2, ZO-1, OCLN, and CLDN4) were decreased by AOM/DSS-treatment; furthermore, this inhibition was rescued by E2 supplementation. The mRNA and protein expression of inflammation-related genes (i.e., KLF4, NF-${\kappa}B$, iNOS, and COX-2) was increased by AOM/DSS-treatment and ameliorated by E2. Conclusions: E2 acts through the estrogen receptor ${\beta}$ signaling pathway to elicit anti-inflammatory effects on intestinal barrier by inducing the expression of MUC2 and tight junction molecules and inhibiting pro-inflammatory cytokines.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.5
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• pp.684-691
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• 2010

The present study was conducted to evaluate the effect of resistant starch (RS) on the large bowel function and plasma lipids in rats with constipation induced by Loperamide. Animals were divided into six groups: normal control-5% cellulose, constipation-5% cellulose, constipation-5% pectin, constipation-5% RS-type 2 (RS2), constipation-8% RS2 and constipation-5% RS type 3 (RS3) groups, and fed experimental diets for five weeks. The results from RS groups were compared with those from other dietary fiber groups. The groups supplemented with RS3 or high level of RS2 showed significantly increased counts of bifidobacteria in the cecum than the other groups. The production of total short chain fatty acids in the cecal contents was significantly high in pectin, RS3 and high RS2 groups. The pH in the cecal contents of the RS supplemented groups was significantly decreased compared with the cellulose supplemented groups. The production of prostaglandin E2 in the colon mucus of the RS groups was higher than the normal group; however, it was significantly decreased compared to the cellulose or pectin supplemented constipated groups. The thickness of the mucus layer and the production of mucus from epithelial cells were significantly increased in RS3 group compared to the constipated cellulose group. Supplementation of resistant starch significantly elevated the ratio of HDL-cholesterol to total cholesterol and significantly lowered plasma atherogenic index compared with cellulose or pectin supplementation in constipated rats. The results of the present study demonstrated that resistant starch supplementation may help in improving the large bowel environment by stimulation of bifidobacterial proliferation, reduction of pH and inflammation factor and by increased production of mucus. It has also been found that an additional health benefit is improvement in lipid levels of serum.