Abstract
The enhanced release of reactive oxygen species from activated neutrophils plays important role in the pathogenesis of inflammatory bowel disease. We previously reported that radon inhalation activates antioxidative functions in various organs of mice. In this study, we examined the protective effects of radon inhalation on dextran sulfate sodium- (DSS) induced colitis in mice which were subjected to DSS for 7 days. Mice were continuously treated with air only (sham) or radon at a concentration of 2000 Bq/m3 from a day before DSS administration to the end of colitis induction. In the results, radon inhalation suppressed the elevation of the disease activity index score and histological damage score induced by DSS. Based on the changes in tumor necrosis factor-alpha in plasma and myeloperoxidase activity in the colon, it was shown that radon inhalation suppressed DSS-induced colonic inflammation. Moreover, radon inhalation suppressed lipid peroxidation of the colon induced by DSS. The antioxidant level (superoxide dismutase and total glutathione) in the colon after DSS administration was significantly higher in mice treated with radon than with the sham. These results suggested that radon inhalation suppressed DSS-induced colitis through the enhancement of antioxidative functions in the colon.
Highlights
Crohn’s disease (CD) and ulcerative colitis (UC) are the two main types of inflammatory bowel disease (IBD), which is chronic inflammatory disease occurring in the intestine
We examined the following biochemical and histological parameters to assess the effects of radon inhalation on dextran sulfate sodium- (DSS)-induced colitis: myeloperoxidase (MPO), nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), SOD, Catalase CD (CAT), total glutathione, lipid peroxide (LPO) level, and histology
There were no significant differences in the water consumption in each group during colitis induction
Summary
Crohn’s disease (CD) and ulcerative colitis (UC) are the two main types of inflammatory bowel disease (IBD), which is chronic inflammatory disease occurring in the intestine. Their etiologies are still unknown, IBD is a substantial health problem in many countries. Once large numbers of neutrophils and macrophages are activated, these cells enter the injured mucosa of the colon, leading to overproduction of reactive oxygen species (ROS) such as superoxide radical (O2−), hydrogen peroxide (H2O2), and hydroxyl radical (OH) [4]. ROS are highly reactive with cell membranes When they are generated close to cell membranes, they induce oxidative stress and oxidized membrane phospholipids (lipid peroxidation) and DNA, which could contribute to gene mutation and inflammation, causing cancer [5]
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