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

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-kappa B (NF-kappa B). This study was performed to explore the effect of emodin on control of the NF-kappa B 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-kappa B subunits, which were correlated with its inhibitory effect on cytoplasmic I kappa B alpha 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-kappa B ligand in bone marrow macrophages. Conclusion. These findings suggest that emodin exerts anti-inflammatory effects in CIA mice through inhibition of the NF-kappa B pathway and therefore may have therapeutic value for the treatment of RA.