Oridonin's therapeutic effect: Suppressing Th1/Th17 simultaneously in a mouse model of Crohn's disease

Abstract

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.