KMID : 0606920130210060435
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Biomolecules & Therapeutics 2013 Volume.21 No. 6 p.435 ~ p.441
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Emodin Isolated from Polygoni cuspidati Radix Inhibits TNF-¥á and IL-6 Release by Blockading NF-¥êB and MAP Kinase Pathways in Mast Cells Stimulated with PMA Plus A23187
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Lu Yue
Jeong Yong-Tae Li Xian Kim Mi-Jin Park Pil-Hoon Hwang Seung-Lark Son Jong-Keun Chang Hyeun-Wook
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Abstract
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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)-¥á 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-¥êB (NF-¥êB) and mitogen-activated protein kinases (MAPKs). Emodin attenuated the nuclear translocation of (NF)-¥êB p65 and its DNA-binding activity by reducing the phosphorylation and degradation of I¥êB¥á and the phosphorylation of I¥êB 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-¥êB activation and of the MAPK pathway.
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KEYWORD
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Emodin, Pro-inflammatory cytokine, NF-¥êB, Mitogen-activated protein kinase, Bone marrow-derived mast cells, PMA plus A23187
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