Citreorosein Inhibits Production of Proinflammatory Cytokines by Blocking Mitogen Activated Protein Kinases, Nuclear Factor-κB and Activator Protein-1 Activation in Mouse Bone Marrow-Derived Mast Cells

Citreorosein Inhibits Production of Proinflammatory Cytokines by Blocking Mitogen Activated Protein Kinases, Nuclear Factor-κB and Activator Protein-1 Activation in Mouse Bone Marrow-Derived Mast Cells

Citreorosein (CIT), an anthraquinone component of Polygoni cuspidate (P.cuspidati) radix, suppressed gene expression of proinflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin(IL)-6 and IL-1β in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate...

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Bibliographic Details
Published in:Biological and Pharmaceutical Bulletin Vol. 35; no. 6; pp. 938 - 945
Main Authors: Yue Lua, Seok-Jong Suhb, Xian Lia, Jing Lu Lianga, Meijuan Chia, Kyoung Hwangboa, Okyun Kwona, Tae-Wook Chungb, Choong-Hwan Kwakb, Kyung-Min Kwonb, Makoto Murakamic, Yurndong Jahnga, Cheorl-Ho Kimb, Jong-Keun Sona, Hyeun Wook Changa
Format: Journal Article
Language:Japanese
Published: Pharmaceutical Society of Japan 01-06-2012
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Summary:Citreorosein (CIT), an anthraquinone component of Polygoni cuspidate (P.cuspidati) radix, suppressed gene expression of proinflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin(IL)-6 and IL-1β in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate 13-acetate (PMA) plus the calcium ionophore A23187. To investigate the molecular mechanisms underlying CIT inhibition of the pro-inflammatory cytokine production, its effects on the activation of both nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) were assessed. CIT attenuated phosphorylation of the MAPKs including extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAP kinase and c-Jun NH2-terminal kinase (JNK). Furthermore, CIT strongly inhibited DNA binding activity of NF-κB through the inhibition of phosphorylation and degradation of inhibitor of kappaB (IκB) as well as activator protein-1 (AP)-1 through the reduction of phosphorylation of c-Jun. These results demonstrate that CIT inhibits proinflammatory cytokines production through the inhibition of both MAPKs and AKT-mediated IκB kinase (IKK) phosphorylation and subsequent inhibition of transcription factor NF-κB activation, thereby attenuating the production of proinflammatory cytokines.
ISSN:0918-6158