Lixuan Sang1, Bing Chang2, Junfeng Zhu3, Fangli Yang4, Yan Li5, Xuefeng Jiang6, Xun Sun7, Changlong Lu8, Danan Wang9. 1. Department of Immunology, China Medical University, Shenyang, China; Department of Geriatrics, First Affiliated Hospital, China Medical University, Shenyang, China. Electronic address: sanglixuan2008@163.com. 2. Department of Gastroenterology, First Affiliated Hospital, China Medical University, Shenyang, China. Electronic address: cb000216@163.com. 3. Department of Immunology, China Medical University, Shenyang, China. Electronic address: zjf0709@126.com. 4. Department of Immunology, China Medical University, Shenyang, China. Electronic address: yfl8412@163.com. 5. Department of Immunology, China Medical University, Shenyang, China. Electronic address: licaorenyanyan@163.com. 6. Department of Immunology, China Medical University, Shenyang, China. Electronic address: cmujxf@hotmail.com. 7. Department of Immunology, China Medical University, Shenyang, China. Electronic address: wsunxun1220@hotmail.com. 8. Department of Immunology, China Medical University, Shenyang, China. Electronic address: cllu@mail.cmu.edu.cn. 9. Department of Immunology, China Medical University, Shenyang, China. Electronic address: wangdanan1972@126.com.
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.
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.