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Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery

Oxidative stress in dermal fibroblasts is strongly correlated with the aging process of the skin. The application of natural compounds that can increase the ability of dermal fibroblasts to counteract oxidative stress is a promising approach to promote skin health and beauty. Eriodictyol is a flavon...

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Autores principales: Buranasudja, Visarut, Muangnoi, Chawanphat, Sanookpan, Kittipong, Halim, Hasseri, Sritularak, Boonchoo, Rojsitthisak, Pornchai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228723/
https://www.ncbi.nlm.nih.gov/pubmed/35745283
http://dx.doi.org/10.3390/nu14122553
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author Buranasudja, Visarut
Muangnoi, Chawanphat
Sanookpan, Kittipong
Halim, Hasseri
Sritularak, Boonchoo
Rojsitthisak, Pornchai
author_facet Buranasudja, Visarut
Muangnoi, Chawanphat
Sanookpan, Kittipong
Halim, Hasseri
Sritularak, Boonchoo
Rojsitthisak, Pornchai
author_sort Buranasudja, Visarut
collection PubMed
description Oxidative stress in dermal fibroblasts is strongly correlated with the aging process of the skin. The application of natural compounds that can increase the ability of dermal fibroblasts to counteract oxidative stress is a promising approach to promote skin health and beauty. Eriodictyol is a flavonoid that exerts several pharmacological actions through its antioxidant properties. However, its protective effects on dermal fibroblasts have not yet been investigated. In this study, we investigated whether eriodictyol protects human dermal fibroblasts (BJ fibroblasts) from the harmful effects of hydrogen peroxide (H(2)O(2)). Eriodictyol pretreatment significantly prevented necrotic cell death caused by H(2)O(2) exposure. In addition, the level of 2′,7′-dichloro-dihydro-fluorescein oxidation was decreased, and that of glutathione was maintained, indicating that the beneficial effects of eriodictyol against H(2)O(2) were closely associated with oxidative-stress attenuation. Eriodictyol mediates its antioxidant effects on dermal fibroblasts against H(2)O(2) through (i) the direct neutralization of reactive oxygen species; (ii) the enhancement of the activities of H(2)O(2)-detoxifying enzymes, including catalase and glutathione peroxidase; and (iii) the induction of the expressions of catalase and glutathione peroxidase 1 via the activation of the Nrf2 signaling system. These results support the potential application of eriodictyol as an ingredient in skincare products for cosmeceutical and pharmaceutical purposes.
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spelling pubmed-92287232022-06-25 Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery Buranasudja, Visarut Muangnoi, Chawanphat Sanookpan, Kittipong Halim, Hasseri Sritularak, Boonchoo Rojsitthisak, Pornchai Nutrients Article Oxidative stress in dermal fibroblasts is strongly correlated with the aging process of the skin. The application of natural compounds that can increase the ability of dermal fibroblasts to counteract oxidative stress is a promising approach to promote skin health and beauty. Eriodictyol is a flavonoid that exerts several pharmacological actions through its antioxidant properties. However, its protective effects on dermal fibroblasts have not yet been investigated. In this study, we investigated whether eriodictyol protects human dermal fibroblasts (BJ fibroblasts) from the harmful effects of hydrogen peroxide (H(2)O(2)). Eriodictyol pretreatment significantly prevented necrotic cell death caused by H(2)O(2) exposure. In addition, the level of 2′,7′-dichloro-dihydro-fluorescein oxidation was decreased, and that of glutathione was maintained, indicating that the beneficial effects of eriodictyol against H(2)O(2) were closely associated with oxidative-stress attenuation. Eriodictyol mediates its antioxidant effects on dermal fibroblasts against H(2)O(2) through (i) the direct neutralization of reactive oxygen species; (ii) the enhancement of the activities of H(2)O(2)-detoxifying enzymes, including catalase and glutathione peroxidase; and (iii) the induction of the expressions of catalase and glutathione peroxidase 1 via the activation of the Nrf2 signaling system. These results support the potential application of eriodictyol as an ingredient in skincare products for cosmeceutical and pharmaceutical purposes. MDPI 2022-06-20 /pmc/articles/PMC9228723/ /pubmed/35745283 http://dx.doi.org/10.3390/nu14122553 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Buranasudja, Visarut
Muangnoi, Chawanphat
Sanookpan, Kittipong
Halim, Hasseri
Sritularak, Boonchoo
Rojsitthisak, Pornchai
Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title_full Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title_fullStr Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title_full_unstemmed Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title_short Eriodictyol Attenuates H(2)O(2)-Induced Oxidative Damage in Human Dermal Fibroblasts through Enhanced Capacity of Antioxidant Machinery
title_sort eriodictyol attenuates h(2)o(2)-induced oxidative damage in human dermal fibroblasts through enhanced capacity of antioxidant machinery
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9228723/
https://www.ncbi.nlm.nih.gov/pubmed/35745283
http://dx.doi.org/10.3390/nu14122553
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