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  • Title: Dextran sulfate sodium-induced acute experimental colitis in C57BL/6 mice is mitigated by selenium.
    Author: Sang L, Chang B, Zhu J, Yang F, Li Y, Jiang X, Sun X, Lu C, Wang D.
    Journal: Int Immunopharmacol; 2016 Oct; 39():359-368. PubMed ID: 27533281.
    Abstract:
    BACKGROUND: Sodium selenite has been shown to have a protective role in experimental colitis. Th1 and Th17 responses are involved in the pathogenesis of dextran sulfate sodium (DSS)-induced colitis and inflammatory bowel disease. This study investigated whether sodium selenite can suppress Th1/Th17-mediated experimental colitis. METHODS: Mice were administered sodium selenite (2μg/g body weight) by gavage daily for 30days. Beginning on day 21, mice were administered 2.5% oral DSS for 9days. The mice were sacrificed on day 31. Survival rates, clinical symptoms, colon lengths, and histological changes were determined. RESULTS: Pretreatment with sodium selenite (2μg/g body weight) improved survival rates, colon shortening, body weight loss, disease activity index, and histopathological score in mice with DSS-induced colitis. Pretreatment with sodium selenite restored interleukin-10 and Foxp3 excretion, as well as reducing the levels of interferon-γ and interleukin-17A. CONCLUSIONS: Pretreatment with sodium selenite showed therapeutic potential for preventing colitis in mice. This effect may be mediated by the immunomodulation of regulatory T cells, expressing anti-inflammatory genes that suppress Th1 and Th17 responses.
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