title: Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice.
abstract: OBJECTIVE
  Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is one of the active components present in the root and rhizome of Rheum palmatum. It has been shown to contain biological activity (antitumour, antibacterial, diuretic and vasorelaxant effects). However, the mechanisms underlying the anti-arthritic effect of emodin have not been elucidated. Here we investigated whether emodin treatment would modulate the severity of the disease in an experimental arthritis model.
  
  
  METHODS
  We evaluated the effects of emodin on CIA mice in vivo.
  
  
  RESULTS
  The pathological processes of RA are mediated by a number of cytokines and MMPs. Expression of these proinflammatory mediators is controlled by nuclear factor-κB (NF-κB). This study was performed to explore the effect of emodin on control of the NF-κB activation pathway and to investigate whether emodin has anti-inflammatory effects in CIA mice in vivo. Emodin inhibited the nuclear translocation and DNA binding of NF-κB subunits, which were correlated with its inhibitory effect on cytoplasmic IκBα degradation in CIA mice. These events further suppressed chemokine production and MMP expression. In addition, emodin inhibited the osteoclast differentiation induced by M-CSF and receptor activation of NF-κB ligand in bone marrow macrophages.
  
  
  CONCLUSIONS
  These findings suggest that emodin exerts anti-inflammatory effects in CIA mice through inhibition of the NF-κB pathway and therefore may have therapeutic value for the treatment of RA.
authors.affiliation: Department of Oral Biochemistry, Wonkwang University, Iksan City, Jeonbuk, South Korea.
authors.forename: Jin-Ki
authors.initials: JK
authors.lastname: Hwang
authors.forename: Eun-Mi
authors.initials: EM
authors.lastname: Noh
authors.forename: Su-Jeong
authors.initials: SJ
authors.lastname: Moon
authors.forename: Jeong-Mi
authors.initials: JM
authors.lastname: Kim
authors.forename: Kang-Beom
authors.initials: KB
authors.lastname: Kwon
authors.forename: Byung-Hyun
authors.initials: BH
authors.lastname: Park
authors.forename: Yong-Ouk
authors.initials: YO
authors.lastname: You
authors.forename: Bo-Mi
authors.initials: BM
authors.lastname: Hwang
authors.forename: Hyeong-Jin
authors.initials: HJ
authors.lastname: Kim
authors.forename: Byeong-Soo
authors.initials: BS
authors.lastname: Kim
authors.forename: Seung-Jin
authors.initials: SJ
authors.lastname: Lee
authors.forename: Jong-Suk
authors.initials: JS
authors.lastname: Kim
authors.forename: Young-Rae
authors.initials: YR
authors.lastname: Lee
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D004642:Emodin / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy*; D007596:Joints / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D021122:Protein Subunits / Q000378:metabolism; D021381:Protein Transport / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D013583:Synovial Membrane / Q000187:drug effects / Q000378:metabolism / Q000473:pathology
chemical_list: D016328:NF-kappa B; D047428:Protein Kinase Inhibitors; D021122:Protein Subunits; D004642:Emodin
keywords: emodin; nuclear factor-κB; rheumatoid arthritis; synoviocytes