KMID : 0352720200440020274
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Journal of Ginseng Research 2020 Volume.44 No. 2 p.274 ~ p.281
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Inhibitory mechanism of ginsenoside Rh3 on granulocyte?macrophage colony-stimulating factor expression in UV-B?irradiated murine SP-1 keratinocytes
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Park Young-Sun
Lee Ji-Eun Park Jong-Il Myung Cheol-Hwan Lim Young-Ho Park Chae-Kyu Hwang Jae-Sung
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Abstract
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Background: Ultraviolet (UV) goes through the epidermis and promotes release of inflammatory cytokines in keratinocytes. Granulocyte?macrophage colony-stimulating factor (GM-CSF), one of the keratinocyte-derived cytokines, regulates proliferation and differentiation of melanocytes. Extracellular signal?regulated kinase (ERK1/2) and protein kinase C (PKC) signaling pathways regulate expression of GM-CSF. Based on these results, we found that ginsenoside Rh3 prevented GM-CSF production and release in UV-B?exposed SP-1 keratinocytes and that this inhibitory effect resulted from the reduction of PKC¥ä and ERK phosphorylation.
Methods: We investigated the mechanism by which ginsenoside Rh3 from Panax ginseng inhibited GM-CSF release from UV-B?irradiated keratinocytes.
Results: Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or UV-B induced release of GM-CSF in the SP-1 keratinocytes. To elucidate whether the change in GM-CSF expression could be related to PKC signaling, the cells were pretreated with H7, an inhibitor of PKC, and irradiated with UV-B. GM-CSF was decreased by H7 in a dose-dependent manner. When we analyzed which ginsenosides repressed GM-CSF expression among 15 ginsenosides, ginsenoside Rh3 showed the largest decline to 40% of GM-CSF expression in enzyme-linked immunosorbent assay. Western blot analysis showed that TPA enhanced the phosphorylation of PKC¥ä and ERK in the keratinocytes. When we examined the effect of ginsenoside Rh3, we identified that ginsenoside Rh3 inhibited the TPA-induced phosphorylation levels of PKC¥ä and ERK.
Conclusion: In summary, we found that ginsenoside Rh3 impeded UV-B?induced GM-CSF production through repression of PKC¥ä and ERK phosphorylation in SP-1 keratinocytes.
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KEYWORD
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Ginsenoside Rh3, GM-CSF, Keratinocytes, PKC, Ultraviolet radiation
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