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KMID : 0624620130460120594
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BMB Reports
2013 Volume.46 No. 12 p.594 ~ p.599
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Binding model for eriodictyol to Jun-N terminal kinase and its anti-inflammatory signaling pathway
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Lee Eun-Jung
Jeong Ki-Woong
Shin A-Reum
Jin Bong-Hwan
Jnawali Hum Nath
Jun Bong-Hyun
Lee Jee-Young
Heo Yong-Seok
Kim Yang-Mee
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Abstract
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The anti-inflammatory activity of eriodictyol and its mode of action were investigated. Eriodictyol suppressed tumor necrosis factor (mTNF)-α, inducible nitric oxide synthase (miNOS), interleukin (mIL)-6, macrophage inflammatory protein (mMIP)-1, and mMIP-2 cytokine release in LPS-stimulated macrophages. We found that the anti-inflammatory cascade of eriodictyol is mediated through the Toll-like Receptor (TLR)4/CD14, p38 mitogen-activated protein kinases (MAPK), extracellular-signal-regulated kinase (ERK), Jun-N terminal kinase (JNK), and cyclooxygenase (COX)-2 pathway. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that eriodictyol exhibits good binding affinity to JNK, 8.79 × 10(5) M(-1). Based on a docking study, we propose a model of eriodictyol and JNK binding, in which eriodictyol forms 3 hydrogen bonds with the side chains of Lys55, Met111, and Asp169 in JNK, and in which the hydroxyl groups of the B ring play key roles in binding interactions with JNK. Therefore, eriodictyol may be a potent anti-inflammatory inhibitor of JNK.
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KEYWORD
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Anti-inflammatory activity, Docking model, Eriodictyol, Flavonoid, STD-NMR
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