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Oridonin's therapeutic effect: Suppressing T h1/ T h17 simultaneously in a mouse model of C rohn's disease
Author(s) -
Wang Shubei,
Zhang Yong,
Saas Philippe,
Wang Haili,
Xu Ying,
Chen Ke,
Zhong Jie,
Yuan Yaozong,
Wang Ying,
Sun Yunwei
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12710
Subject(s) - colitis , medicine , cancer research , immunology , inflammatory bowel disease , pharmacology , microbiology and biotechnology , tumor necrosis factor alpha , biology , disease , pathology
Abstract Background and Aim C rohn's disease is a chronic inflammatory bowel disease. Oridonin is an effective component isolated from R abdosia rubescens. It can inhibit the activation of transcription factor nuclear factor‐kappa B and suppress the over expression of cytokines. We postulated that oridonin may be a potential therapeutic candidate for C rohn's disease. Methods To confirm the postulation, we investigated clinical and immunologic modulations of oridonin in a mouse model of trinitrobenzene sulfonic acid‐induced colitis. Results It was found that oridonin attenuated trinitrobenzene sulfonic acid‐induced colitis as represented by a reduction in colonic interferon‐γ/inteleukin‐17 secretion and a decrement in splenic T h1/ T h17 cells and effector memory CD 4 + T cells. Oridonin treatment inhibited the proliferation of CD 4 + T cells and upregulated the apoptosis of lymphocytes by inhibiting nuclear translocation of transcription factor nuclear factor‐kappa B . Conclusions Oridonin is a potential modulator for trinitrobenzene sulfonic acid‐induced colitis and other T h1/ T h17 mediated inflammatory diseases.