Abstract
ABSTRACTPurpose:To evaluate the effects of sucralfate enemas in tissue contents of E-cadherin and ?-catenin in an experimental diversion colitis.Methods:Thirty-six male Wistar rats were submitted to a proximal colostomy and a distal mucous fistula. They were allocated into three groups: first group received daily saline enemas (2 mL/day) and the two other groups daily enemas with sucralfate at dosage of 1 or 2 g/kg/day, respectively. Six animals of each group were euthanized after two weeks and six animals after four weeks. The inflammation of the excluded mucosa was evaluated by histological analysis. The oxidative damage was quantified by measurement of malondialdehyde tissue levels. The expression of E-cadherin and ?-catenin was identified by immunohistochemistry, and its contents were quantified by computer-assisted image analysis.Results:Sucralfate enemas reduced inflammation in animals subjected to treatment with 2 g/kg/day by four weeks, and the levels of oxidative damage in mucosa without fecal stream irrespective of concentration and time of intervention. E-cadherin and ?-catenin content increased in segments without fecal stream in those animals subjected to treatment with sucralfate.Conclusions:Sucralfate reduces the inflammation and oxidative stress and increases the tissue content of E-cadherin and ?-catenin in colonic mucosa devoid to the fecal stream.
Highlights
The integrity of the colonic epithelium is essential for the maintenance of human life[1]
Disruption of epithelial barrier integrity is a significant factor associated with the development of several diseases, including gastroenteritis caused by viruses or bacteria, necrotizing enterocolitis, inflammatory bowel disease (IBD), and diversion colitis (DC)[2,3,4,5]
The mechanism of defense of the epithelial barrier is formed by a layer of specialized and polarized epithelial cells, a mucus tier that covers the intestinal mucosa, intercellular junction systems formed by tight junctions (TJs), adherens junctions (AJs), gap junctions, desmosomes, and a basal membrane
Summary
The integrity of the colonic epithelium is essential for the maintenance of human life[1]. DC is an inflammatory process that occurs in colon or rectal mucosa devoid of the intestinal transit[6] It has been recognized as an energy-deficiency syndrome caused by a lack of short-chain fatty acids (SCFAs) supply to colonic epithelial cells[6,7]. When there is deficiency of SCFAs, the cells of the colonic mucosa present alterations in their redox state with a decrease in cellular oxidative phosphorylation, resulting in overproduction of reactive oxygen species (ROS), which causes oxidative damage to all defense systems of the epithelial barrier[5,7]. Luminal deficiency of SCFAs exacerbates DC, whereas supplying the colonic mucosa that is excluded from the fecal stream with nutritional solutions rich in SCFAs improves the trophism of the epithelium, reduces the levels of oxidative tissue damage, increases the synthesis of several proteins, and protects the colonic mucosa against the inflammatory process[9,10]
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