Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice

Jin Ki Hwang, Eun Mi Noh, Su Jeong Moon, Jeong Mi Kim, Kang Beom Kwon, Byung Hyun Park, Yong Ouk You, Bo Mi Hwang, Hyeong Jin Kim, Byeong Soo Kim, Seung Jin Lee, Jong Suk Kim, Young Rae Lee

Research output: Contribution to journalArticlepeer-review

81 Scopus citations


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.Conclusion. 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.

Original languageEnglish
Article numberket178
Pages (from-to)1583-1591
Number of pages9
JournalRheumatology (United Kingdom)
Issue number9
StatePublished - Sep 2013

Bibliographical note

Funding Information:
Funding: This work was supported in part by a National Research Foundation of Korea (NRF) grant funded by the Korean Government (MEST) (No. 2009-0076698 and No. 2011-0030716), Republic of Korea.


  • Emodin
  • Nuclear factor-κB
  • Rheumatoid arthritis
  • Synoviocytes


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