Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice
Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice
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DOI：
10.1093/rheumatology/ket178
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发表时间：
2013-09-01
期刊：
影响因子：
5.5
通讯作者：
Lee, Young-Rae
中科院分区：
文献类型：
--
作者：
Hwang, Jin-Ki;Noh, Eun-Mi;Lee, Young-Rae
方法。我们在体内评价了大黄素对CIA小鼠的影响。RA的病理过程是由多种细胞因子和MMPs介导的。这些促炎介质的表达受核因子κ B （nf - κ B）的控制。本实验旨在探讨大黄素对CIA小鼠体内nf - κ B激活通路的调控作用，并探讨大黄素是否具有抗炎作用。大黄素抑制nf - κ B亚基的核易位和DNA结合，这与大黄素抑制CIA小鼠胞质I κ B α降解有关。这些事件进一步抑制趋化因子的产生和MMP的表达。此外，大黄素还能抑制骨髓巨噬细胞M-CSF诱导的破骨细胞分化和nf - κ B配体受体的激活。这些发现提示，大黄素通过抑制nf - κ B通路在CIA小鼠中发挥抗炎作用，因此可能具有治疗RA的治疗价值。
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.