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Updated: Mar 16, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Dextran sulfate sodium-induced acute experimental colitis in C57BL/6 mice is mitigated by selenium
Lixuan Sang1, Bing Chang2, Junfeng Zhu3
1Department of Immunology, China Medical University, Shenyang, China; Department of Geriatrics, First Affiliated Hospital, China Medical University, Shenyang, China.
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.
