Inhibitory Effect of Panduratin A on UV-induced Activation of Mitogen-Activated Protein Kinases (MAPKs) in Dermal Fibroblast Cells
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作者:
Shim, Jae-Seok
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Yonsei Univ, Dept Biomat Sci & Engn, Seoul 120749, South KoreaYonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
Shim, Jae-Seok
[2
]
Kwon, Yi-Young
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Yonsei Univ, Dept Biotechnol, Seoul 120749, South KoreaYonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
Kwon, Yi-Young
[1
]
Han, Young-Sun
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Yonsei Univ, Dept Biotechnol, Seoul 120749, South KoreaYonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
Han, Young-Sun
[1
]
Hwang, Jae-Kwan
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Yonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
Yonsei Univ, Dept Biomat Sci & Engn, Seoul 120749, South KoreaYonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
Hwang, Jae-Kwan
[1
,2
]
机构:
[1] Yonsei Univ, Dept Biotechnol, Seoul 120749, South Korea
[2] Yonsei Univ, Dept Biomat Sci & Engn, Seoul 120749, South Korea
Exposure of the skin to ultraviolet (UV) induces photoaging associated with up-regulated matrix metalloproteinases (MMPs) activities and decreased collagen synthesis. We previously reported that panduratin A, a chalcone compound isolated from Kaempferia pandurata Roxb., decreased MMP-1 expression in UV-irradiated human skin fibroblasts. Here, we have investigated the effect of panduratin A on UV-induced activation of mitogen-activated protein kinases (MAPKs) signaling modules such as extracellular-regulated protein kinase (ERK), Jun-N-terminal kinase (JNK) and p38 kinase. Treatment with panduratin A in the range of 0.001 -0.1 mu M significantly inhibited UV-induced ERK, JNK and p38 activation. Moreover, inhibition of ERK, JNK and p38 by panduratin A resulted in decreased c-Fos expression and c-Jun phosphorylation induced by UV, which led to inhibition of activator protein-1 (AP-1) DNA binding activity. Panduratin A showed stronger activity than epigallocatechin 3-O-gallate (EGCG) known as a natural anti-aging agent. The results suggest that panduratin A can down-regulate UV-induced MMP-1 expression by inhibiting the MAPKs pathways and AP-1 activation.