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KMID : 1123920070210041017
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Korean Journal of Oriental Physiology and Pathology
2007 Volume.21 No. 4 p.1017 ~ p.1024
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Wogonin inhibits Cytokine-induced TARC/CCL17 Expression by Suppression of NF- activation via p38 MAP kinase Signalning Pathways in HaCaT Keratinocytes
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Jang Seon-Il
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Abstract
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Thymus and activation-regulated chemokine (TARC/CCL-17), produced by keratinocytes, is a CC chemokine known to selectively Th2 type T cells via and is implicated in the development of atopic dermatitis (AD). TARC/CCL17 expression was induced by cytokines such as tumor necrosis factor- (TNF-) and interferon- (IFN-). We recently found that the wogonin, a flavone isolated from Scutellaria baicalensis, suppressed TARC expression via heme oxygenase 1 (HO1) in human keratinocytes induced with mite antigen. However, little is known about the inhibitory mechanism of wogonin on TARC/CCL-17 expression stimulated with cytokines. To investigate the inhibitory mechanism, I determined the inhibitory effects of wogonin on the activation of nuclear factor- (NF-) and phosphorylation, and also examined the activation of p38 MAP kainase in HaCaT keratinocytes stimulated with TNF- and IFN-. Wogonin inhibited NF--DNA complex, NF- binding activity, and the phosphorylation of in a dose dependent manner. Wogonin also inhibited the translocation of NF- from cytosol to nucleus. Moreover, the phosphorylation of of p38 MAP kinase in the TNF- and IFN--stimulated HaCaT keratinocytes were suppressed by wogonin in a dose dependent manner. These results suggest that wogonin may inhibit cytokine-induced NF- activation by degradation via suppression of p38 MAP kinase signaling pathway in keratinocytes and modulation of wogonin signaling pathway may be beneficial for the treatment of AD.
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KEYWORD
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Atopic dermatitis, TARC/CCL17, NF-, TNF-, IFN-, HaCaT keratinocytes
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