Oridonin's therapeutic effect: suppressing Th1/Th17 simultaneously in a mouse model of Crohn's disease.
BACKGROUND AND AIM
Crohn's disease is a chronic inflammatory bowel disease. Oridonin is an effective component isolated from Rabdosia 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 Crohn'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 Th1/Th17 cells and effector memory CD4(+) T cells. Oridonin treatment inhibited the proliferation of CD4(+) 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 Th1/Th17 mediated inflammatory diseases.
['Wang|Shubei|S|', 'Zhang|Yong|Y|', 'Saas|Philippe|P|', 'Wang|Haili|H|', 'Xu|Ying|Y|', 'Chen|Ke|K|', 'Zhong|Jie|J|', 'Yuan|Yaozong|Y|', 'Wang|Ying|Y|', 'Sun|Yunwei|Y|']
D000818:Animals D017209:Apoptosis D002478:Cells, Cultured D003424:Crohn Disease D004195:Disease Models, Animal D045786:Diterpenes, Kaurane D007371:Interferon-gamma D020381:Interleukin-17 D008297:Male D008807:Mice, Inbred BALB C D016328:NF-kappa B D008517:Phytotherapy D013154:Spleen D018417:Th1 Cells D058504:Th17 Cells D014302:Trinitrobenzenesulfonic Acid D015854:Up-Regulation
oridonin cytokines animal models