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Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage
Ultraviolet B (UVB) radiation induces skin damage, skin matrix degradation, and wrinkle formation through photochemical reaction and oxidative stress. Therefore, protecting the skin from UVB can prevent skin aging. In this study, we investigated the effects of a mixture (RA) of Rg2, a ginsenoside, a...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Taylor & Francis
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282468/ https://www.ncbi.nlm.nih.gov/pubmed/30533262 http://dx.doi.org/10.1080/19768354.2018.1523806 |
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author | Chung, Yu Heon Jeong, Seul A. Choi, Hyun Seok Ro, Seungil Lee, Jung Sup Park, Jong Kun |
author_facet | Chung, Yu Heon Jeong, Seul A. Choi, Hyun Seok Ro, Seungil Lee, Jung Sup Park, Jong Kun |
author_sort | Chung, Yu Heon |
collection | PubMed |
description | Ultraviolet B (UVB) radiation induces skin damage, skin matrix degradation, and wrinkle formation through photochemical reaction and oxidative stress. Therefore, protecting the skin from UVB can prevent skin aging. In this study, we investigated the effects of a mixture (RA) of Rg2, a ginsenoside, and astaxanthin, an antioxidant, on the responses of HaCaT cells exposed to UVB (700 J/m(2)). The cells were incubated for 24 h after UVB exposure and cell viability was determined by MTT assay. UVB decreased cell viability by 60% compared to that of untreated control cells, whereas RA increased cell viability in a concentration-dependent manner, and this increase was significantly higher than that in the single treatment groups. Further, UVB increased the levels of DNA lesions such as cyclobutane pyrimidine dimer (CPD) and 8-hydroxyguanine (8-OHdG). Conversely, RA decreased both CPD and 8-OHdG levels in a concentration-dependent manner. UVB exposure also increased phosphorylation of ataxia-telangiectasia mutated (ATM) protein kinase and p53 and subsequently increased the levels of GADD45α, p21, and matrix metalloproteinases (MMPs)-3, -9, and -13. Additionally, UVB exposure decreased the level of COL1A1. However, RA treatment decreased the levels of p-ATM, p-p53, GADD45α, p21, MMP-3, -9, and -13 and increased the level of COL1A1 in a concentration-dependent manner. These results suggest that RA reduces UVB-induced cytotoxicity and genotoxicity through up-regulation of DNA repair via the combined effects of Rg2 and astaxanthin. |
format | Online Article Text |
id | pubmed-6282468 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-62824682018-12-07 Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage Chung, Yu Heon Jeong, Seul A. Choi, Hyun Seok Ro, Seungil Lee, Jung Sup Park, Jong Kun Anim Cells Syst (Seoul) Translational Medicine Ultraviolet B (UVB) radiation induces skin damage, skin matrix degradation, and wrinkle formation through photochemical reaction and oxidative stress. Therefore, protecting the skin from UVB can prevent skin aging. In this study, we investigated the effects of a mixture (RA) of Rg2, a ginsenoside, and astaxanthin, an antioxidant, on the responses of HaCaT cells exposed to UVB (700 J/m(2)). The cells were incubated for 24 h after UVB exposure and cell viability was determined by MTT assay. UVB decreased cell viability by 60% compared to that of untreated control cells, whereas RA increased cell viability in a concentration-dependent manner, and this increase was significantly higher than that in the single treatment groups. Further, UVB increased the levels of DNA lesions such as cyclobutane pyrimidine dimer (CPD) and 8-hydroxyguanine (8-OHdG). Conversely, RA decreased both CPD and 8-OHdG levels in a concentration-dependent manner. UVB exposure also increased phosphorylation of ataxia-telangiectasia mutated (ATM) protein kinase and p53 and subsequently increased the levels of GADD45α, p21, and matrix metalloproteinases (MMPs)-3, -9, and -13. Additionally, UVB exposure decreased the level of COL1A1. However, RA treatment decreased the levels of p-ATM, p-p53, GADD45α, p21, MMP-3, -9, and -13 and increased the level of COL1A1 in a concentration-dependent manner. These results suggest that RA reduces UVB-induced cytotoxicity and genotoxicity through up-regulation of DNA repair via the combined effects of Rg2 and astaxanthin. Taylor & Francis 2018-10-09 /pmc/articles/PMC6282468/ /pubmed/30533262 http://dx.doi.org/10.1080/19768354.2018.1523806 Text en © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Translational Medicine Chung, Yu Heon Jeong, Seul A. Choi, Hyun Seok Ro, Seungil Lee, Jung Sup Park, Jong Kun Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title | Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title_full | Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title_fullStr | Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title_full_unstemmed | Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title_short | Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage |
title_sort | protective effects of ginsenoside rg2 and astaxanthin mixture against uvb-induced dna damage |
topic | Translational Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282468/ https://www.ncbi.nlm.nih.gov/pubmed/30533262 http://dx.doi.org/10.1080/19768354.2018.1523806 |
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