Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes
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 sig...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2020-03-01
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| Series: | Journal of Ginseng Research |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1226845318302562 |
| _version_ | 1818358788718067712 |
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| author | Young Sun Park Ji Eun Lee Jong Il Park Cheol hwan Myung Young-Ho Lim Chae Kyu Park Jae Sung Hwang |
| author_facet | Young Sun Park Ji Eun Lee Jong Il Park Cheol hwan Myung Young-Ho Lim Chae Kyu Park Jae Sung Hwang |
| author_sort | Young Sun Park |
| collection | DOAJ |
| description | 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 PKCδ 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 PKCδ 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 PKCδ and ERK. Conclusion: In summary, we found that ginsenoside Rh3 impeded UV-B–induced GM-CSF production through repression of PKCδ and ERK phosphorylation in SP-1 keratinocytes. Keywords: Ginsenoside Rh3, GM-CSF, Keratinocytes, PKC, Ultraviolet radiation |
| first_indexed | 2024-12-13T20:34:34Z |
| format | Article |
| id | doaj.art-028afa9557d84e7fab8338f7c8b9ed7d |
| institution | Directory Open Access Journal |
| issn | 1226-8453 |
| language | English |
| last_indexed | 2024-12-13T20:34:34Z |
| publishDate | 2020-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Ginseng Research |
| spelling | doaj.art-028afa9557d84e7fab8338f7c8b9ed7d2022-12-21T23:32:20ZengElsevierJournal of Ginseng Research1226-84532020-03-01442274281Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytesYoung Sun Park0Ji Eun Lee1Jong Il Park2Cheol hwan Myung3Young-Ho Lim4Chae Kyu Park5Jae Sung Hwang6Department of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of KoreaDepartment of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of KoreaDepartment of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of KoreaDepartment of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of KoreaKGC R&D Headquarters, Daejeon, Republic of KoreaKGC R&D Headquarters, Daejeon, Republic of KoreaDepartment of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of Korea; Corresponding author. Department of Genetic Engineering & Graduate School of Biotechnology, Kyung Hee University, Yongin-si, Gyeonggi-do, 17104, Republic of KoreaBackground: 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 PKCδ 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 PKCδ 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 PKCδ and ERK. Conclusion: In summary, we found that ginsenoside Rh3 impeded UV-B–induced GM-CSF production through repression of PKCδ and ERK phosphorylation in SP-1 keratinocytes. Keywords: Ginsenoside Rh3, GM-CSF, Keratinocytes, PKC, Ultraviolet radiationhttp://www.sciencedirect.com/science/article/pii/S1226845318302562 |
| spellingShingle | Young Sun Park Ji Eun Lee Jong Il Park Cheol hwan Myung Young-Ho Lim Chae Kyu Park Jae Sung Hwang Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes Journal of Ginseng Research |
| title | Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes |
| title_full | Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes |
| title_fullStr | Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes |
| title_full_unstemmed | Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes |
| title_short | Inhibitory mechanism of ginsenoside Rh3 on granulocyte–macrophage colony-stimulating factor expression in UV-B–irradiated murine SP-1 keratinocytes |
| title_sort | inhibitory mechanism of ginsenoside rh3 on granulocyte macrophage colony stimulating factor expression in uv b irradiated murine sp 1 keratinocytes |
| url | http://www.sciencedirect.com/science/article/pii/S1226845318302562 |
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