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http://dx.doi.org/10.4062/biomolther.2013.068

Emodin Isolated from Polygoni cuspidati Radix Inhibits TNF-α and IL-6 Release by Blockading NF-κB and MAP Kinase Pathways in Mast Cells Stimulated with PMA Plus A23187  

Lu, Yue (School of Pharmacy, Shanghai University of Traditional Chinese Medicine)
Jeong, Yong-Tae (College of Pharmacy, Yeungnam University)
Li, Xian (College of Pharmacy, Yeungnam University)
Kim, Mi Jin (College of Pharmacy, Yeungnam University)
Park, Pil-Hoon (College of Pharmacy, Yeungnam University)
Hwang, Seung-Lark (College of Pharmacy, Yeungnam University)
Son, Jong Keun (College of Pharmacy, Yeungnam University)
Chang, Hyeun Wook (College of Pharmacy, Yeungnam University)
Publication Information
Biomolecules & Therapeutics / v.21, no.6, 2013 , pp. 435-441 More about this Journal
Abstract
Emodin, a naturally occurring anthraquinone derivative isolated from Polygoni cuspidati radix, has several beneficial pharmacologic effects, which include anti-cancer, anti-diabetic, and anti-inflammatory activities. In this study, the authors examined the effect of emodin on the production of proinflammatory cytokines, such as, tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6, in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate 13-acetate (PMA) plus the calcium ionophore A23187. To investigate the mechanism responsible for the regulation of pro-inflammatory cytokine production by emodin, the authors assessed its effects on the activations of transcriptional factor nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and mitogen-activated protein kinases (MAPKs). Emodin attenuated the nuclear translocation of (NF)-${\kappa}B$ p65 and its DNA-binding activity by reducing the phosphorylation and degradation of $I{\kappa}B{\alpha}$ and the phosphorylation of $I{\kappa}B$ kinase B (IKK). Furthermore, emodin dose-dependently attenuated the phosphorylations of MAPKs, such as, extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAP kinase, and the stress-activated protein kinases (SAPK)/c-Jun-N-terminal kinase (JNK). Taken together, the findings of this study suggest that the anti-inflammatory effects of emodin on PMA plus A23187-stimulated BMMCs are mediated via the inhibition of NF-${\kappa}B$ activation and of the MAPK pathway.
Keywords
Emodin; Pro-inflammatory cytokine; NF-${\kappa}B$; Mitogen-activated protein kinase; Bone marrow-derived mast cells; PMA plus A23187;
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