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Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence
BACKGROUND: Malvidin is one of the most abundant components in red wines and black rice. The effects of malvidin on aging and lifespan under oxidative stress have not been fully understood. This study focused on the anti-aging effect of malvidin on stress-induced premature senescence (SIPS) in WI-38...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society of Cancer Prevention
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4819664/ https://www.ncbi.nlm.nih.gov/pubmed/27051647 http://dx.doi.org/10.15430/JCP.2016.21.1.32 |
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author | Seo, Hye Rin Choi, Mi Jin Choi, Ji Myung Ko, Jong Cheol Ko, Jee Yeon Cho, Eun Ju |
author_facet | Seo, Hye Rin Choi, Mi Jin Choi, Ji Myung Ko, Jong Cheol Ko, Jee Yeon Cho, Eun Ju |
author_sort | Seo, Hye Rin |
collection | PubMed |
description | BACKGROUND: Malvidin is one of the most abundant components in red wines and black rice. The effects of malvidin on aging and lifespan under oxidative stress have not been fully understood. This study focused on the anti-aging effect of malvidin on stress-induced premature senescence (SIPS) in WI-38 human lung-derived diploid fibroblasts. METHODS: In order to determine the viability of WI-38 cells, MTT assay was conducted, and malondialdehyde level was determined using thiobarbituric acid-reactive substance assay. Protein expression of inflammation-related factors was also evaluated by Western blot analysis. RESULTS: Acute and chronic oxidative stress via hydrogen peroxide (H(2)O(2)) treatment led to SIPS in WI-38 cells, which showed decreased cell viability, increased lipid peroxidation, and a shortened lifespan in comparison with non-H(2)O(2)-treated WI-38 cells. However, malvidin treatment significantly attenuated H(2)O(2)-induced oxidative stress by inhibiting lipid peroxidation and increasing cell viability. Furthermore, the lifespan of WI-38 cells was prolonged by malvidin treatment. In addition, malvidin downregulated the expression of oxidative stress-related proteins, including NF-κB, COX-2, and inducible nitric oxide synthase. Furthermore, protein expression levels of p53, p21, and Bax were also regulated by malvidin treatment in WI-38 cells undergoing SIPS. CONCLUSIONS: Malvidin may potentially inhibit the aging process by controlling oxidative stress. |
format | Online Article Text |
id | pubmed-4819664 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Korean Society of Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-48196642016-04-05 Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence Seo, Hye Rin Choi, Mi Jin Choi, Ji Myung Ko, Jong Cheol Ko, Jee Yeon Cho, Eun Ju J Cancer Prev Original Article BACKGROUND: Malvidin is one of the most abundant components in red wines and black rice. The effects of malvidin on aging and lifespan under oxidative stress have not been fully understood. This study focused on the anti-aging effect of malvidin on stress-induced premature senescence (SIPS) in WI-38 human lung-derived diploid fibroblasts. METHODS: In order to determine the viability of WI-38 cells, MTT assay was conducted, and malondialdehyde level was determined using thiobarbituric acid-reactive substance assay. Protein expression of inflammation-related factors was also evaluated by Western blot analysis. RESULTS: Acute and chronic oxidative stress via hydrogen peroxide (H(2)O(2)) treatment led to SIPS in WI-38 cells, which showed decreased cell viability, increased lipid peroxidation, and a shortened lifespan in comparison with non-H(2)O(2)-treated WI-38 cells. However, malvidin treatment significantly attenuated H(2)O(2)-induced oxidative stress by inhibiting lipid peroxidation and increasing cell viability. Furthermore, the lifespan of WI-38 cells was prolonged by malvidin treatment. In addition, malvidin downregulated the expression of oxidative stress-related proteins, including NF-κB, COX-2, and inducible nitric oxide synthase. Furthermore, protein expression levels of p53, p21, and Bax were also regulated by malvidin treatment in WI-38 cells undergoing SIPS. CONCLUSIONS: Malvidin may potentially inhibit the aging process by controlling oxidative stress. Korean Society of Cancer Prevention 2016-03 2016-03-30 /pmc/articles/PMC4819664/ /pubmed/27051647 http://dx.doi.org/10.15430/JCP.2016.21.1.32 Text en Copyright © 2016 Korean Society of Cancer Prevention This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial 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 | Original Article Seo, Hye Rin Choi, Mi Jin Choi, Ji Myung Ko, Jong Cheol Ko, Jee Yeon Cho, Eun Ju Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title | Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title_full | Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title_fullStr | Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title_full_unstemmed | Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title_short | Malvidin Protects WI-38 Human Fibroblast Cells Against Stress-induced Premature Senescence |
title_sort | malvidin protects wi-38 human fibroblast cells against stress-induced premature senescence |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4819664/ https://www.ncbi.nlm.nih.gov/pubmed/27051647 http://dx.doi.org/10.15430/JCP.2016.21.1.32 |
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