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

• Published in: Biomolecules & therapeutics Vol. 21; no. 6; pp. 435 - 441
• Main Authors: Lu, Yue, Jeong, Yong-Tae, Li, Xian, Kim, Mi Jin, Park, Pil-Hoon, Hwang, Seung-Lark, Son, Jong Keun, Chang, Hyeun Wook
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Society of Applied Pharmacology 01.11.2013; 한국응용약물학회
• Subjects: 약학; Emodin; Mitogen-activated protein kinase; NF-κB; Pro-inflammatory cytokine; PMA plus A23187; Bone marrow-derived mast cells
• ISSN: 1976-9148; 2005-4483
• DOI: 10.4062/biomolther.2013.068

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)-α 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-κB (NF-κB) and mitogen-activated protein kinases (MAPKs). Emodin attenuated the nuclear translocation of (NF)-κB p65 and its DNA-binding activity by reducing the phosphorylation and degradation of IκBα and the phosphorylation of IκB 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-κB activation and of the MAPK pathway.