title: Oridonin's therapeutic effect: suppressing Th1/Th17 simultaneously in a mouse model of Crohn's disease.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine.
authors.forename: Shubei
authors.initials: S
authors.lastname: Wang
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Philippe
authors.initials: P
authors.lastname: Saas
authors.forename: Haili
authors.initials: H
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Xu
authors.forename: Ke
authors.initials: K
authors.lastname: Chen
authors.forename: Jie
authors.initials: J
authors.lastname: Zhong
authors.forename: Yaozong
authors.initials: Y
authors.lastname: Yuan
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Yunwei
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002478:Cells, Cultured; D003424:Crohn Disease / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology*; D004195:Disease Models, Animal; D045786:Diterpenes, Kaurane / Q000494:pharmacology* / Q000627:therapeutic use*; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D008297:Male; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000235:genetics; D008517:Phytotherapy; D013154:Spleen / Q000166:cytology / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*; D014302:Trinitrobenzenesulfonic Acid; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D045786:Diterpenes, Kaurane; D020381:Interleukin-17; D016328:NF-kappa B; C011959:oridonin; D007371:Interferon-gamma; D014302:Trinitrobenzenesulfonic Acid
keywords: animal models; cytokines; oridonin