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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...

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Autores principales: Seo, Hye Rin, Choi, Mi Jin, Choi, Ji Myung, Ko, Jong Cheol, Ko, Jee Yeon, Cho, Eun Ju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society of Cancer Prevention 2016
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.
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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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