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Inhibitory mechanism of Korean Red Ginseng on GM-CSF expression in UVB-irradiated keratinocytes

  • Chung, Ira (Department of Genetic Engineering and the Graduate School of Biotechnology, Kyung Hee University) ;
  • Lee, Jieun (Department of Genetic Engineering and the Graduate School of Biotechnology, Kyung Hee University) ;
  • Park, Young Sun (Department of Genetic Engineering and the Graduate School of Biotechnology, Kyung Hee University) ;
  • Lim, Yeji (Eunkwang Girl's High School) ;
  • Chang, Do Hyeon (Gyeonggi Science High School for the Gifted) ;
  • Park, Jongil (Department of Genetic Engineering and the Graduate School of Biotechnology, Kyung Hee University) ;
  • Hwang, Jae Sung (Department of Genetic Engineering and the Graduate School of Biotechnology, Kyung Hee University)
  • Received : 2014.09.19
  • Accepted : 2015.03.03
  • Published : 2015.10.15

Abstract

Background: UV-irradiated keratinocytes secrete various proinflammatory cytokines. UV-induced skin damage is mediated by growth factors and proinflammatory cytokines such as granulocyte macrophage colony stimulating factor (GM-CSF). In a previous study, we found that the saponin of Korean Red Ginseng (SKRG) decreased the expression of GM-CSF in UVB-irradiated SP-1 keratinocytes. In this study, we attempted to find the inhibitory mechanism of SKRG on UVB-induced GM-CSF expression in SP-1 keratinocytes. Methods: We investigated the inhibitory mechanism of SKRG and ginsenosides from Panax ginseng on UVB-induced GM-CSF expression in SP-1 keratinocytes. Results: Treatment with SKRG decreased the expression of GM-CSF mRNA and protein induced by irradiation of UVB in SP-1 keratinocytes. The phosphorylation of ERK was induced by UVB at 10 min, and decreased with SKRG treatment in SP-1 keratinocytes. In addition, treatment with SKRG inhibited the UVB-induced phosphorylation of epidermal growth factor receptor (EGFR), which is known to be an upstream signal of ERK. From these results, we found that the inhibition of GM-CSF expression by SKRG was derived from the decreased phosphorylation of EGFR. To identify the specific compound composing SKRG, we tested fifteen kinds of ginsenosides. Among these compounds, ginsenoside-Rh3 decreased the expression of GM-CSF protein and mRNA in SP-1 keratinocytes. Conclusion: Taken together, we found that treatment with SKRG decreased the phosphorylation of EGFR and ERK in UVB-irradiated SP-1 keratinocytes and subsequently inhibited the expression of GM-CSF. Furthermore, we identified ginsenoside-Rh3 as the active saponin in Korean Red Ginseng.

Keywords

References

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