Liu Xiuhong1,2, D U Yajun1,2, Liu Guoxing1,2, Dan Guomei1,2, Tong Xin2, Xiao Juan2. 1. Zaoyang First People's Hospital (Affiliated Zaoyang Hospital of Hubei University of Arts and Science), Xiangyang 441200, China. 2. Laboratory of Molecular Medicine, Hubei University of Arts and Science, Xiangyang 441053, China.
Abstract
OBJECTIVE: To investigate whether kirenol, the major pharmacologically active compound of the Chinese medicinal herb Herba Siegesbeckiae, can protect mice from dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). METHODS: C57BL/6 mice with or without kirenol pretreatment were treated with DSS in drinking water for 7 days to induce UC. The symptoms of UC including weight loss, diarrhea and bloody stool were observed daily and graded using the disease activity index (DAI). Colon injury of the mice was assessed by measuring the length of the colon and HE staining of the colon tissue. The levels of inflammatory cytokines produced by the mesenteric lymph nodes (MLNs) lymphocytes were measured using enzyme-linked immunosorbent assay; the apoptosis of the lymphocytes and CD4+ T cells was analyzed using flow cytometry. RESULTS: The mice receiving pretreatment with kirenol showed obviously ameliorated symptoms of UC and milder pathological changes in the colon as compared with the control mice. Kirenol treatment significantly down-regulated the secretion of IFN-γ, IL-17A, IL-6 and TNF-α by the MLNs lymphocytes and increased the apoptosis of lymphocytes, especially CD4+ T cells in the DSS-treated mice. CONCLUSIONS: Kirenol can protect against T cell-mediated colon injury in DSS-treated mice possibly by suppressing the secretion of inflammatory mediators and inducing apoptosis of the inflammatory lymphocytes.
OBJECTIVE: To investigate whether kirenol, the major pharmacologically active compound of the Chinese medicinal herb Herba Siegesbeckiae, can protect mice from dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). METHODS: C57BL/6 mice with or without kirenol pretreatment were treated with DSS in drinking water for 7 days to induce UC. The symptoms of UC including weight loss, diarrhea and bloody stool were observed daily and graded using the disease activity index (DAI). Colon injury of the mice was assessed by measuring the length of the colon and HE staining of the colon tissue. The levels of inflammatory cytokines produced by the mesenteric lymph nodes (MLNs) lymphocytes were measured using enzyme-linked immunosorbent assay; the apoptosis of the lymphocytes and CD4+ T cells was analyzed using flow cytometry. RESULTS: The mice receiving pretreatment with kirenol showed obviously ameliorated symptoms of UC and milder pathological changes in the colon as compared with the control mice. Kirenol treatment significantly down-regulated the secretion of IFN-γ, IL-17A, IL-6 and TNF-α by the MLNs lymphocytes and increased the apoptosis of lymphocytes, especially CD4+ T cells in the DSS-treated mice. CONCLUSIONS:Kirenol can protect against T cell-mediated colon injury in DSS-treated mice possibly by suppressing the secretion of inflammatory mediators and inducing apoptosis of the inflammatory lymphocytes.
Authors: Ana M Dias; Alexandra Correia; Márcia S Pereira; Catarina R Almeida; Inês Alves; Vanda Pinto; Telmo A Catarino; Nuno Mendes; Magdalena Leander; M Teresa Oliva-Teles; Luís Maia; Cristina Delerue-Matos; Naoyuki Taniguchi; Margarida Lima; Isabel Pedroto; Ricardo Marcos-Pinto; Paula Lago; Celso A Reis; Manuel Vilanova; Salomé S Pinho Journal: Proc Natl Acad Sci U S A Date: 2018-05-02 Impact factor: 11.205