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Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter

Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava...

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Autores principales: Ha, Jae Won, Song, Hyerim, Hong, Seong Su, Boo, Yong Chool
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6617419/
https://www.ncbi.nlm.nih.gov/pubmed/31234405
http://dx.doi.org/10.3390/antiox8060190
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author Ha, Jae Won
Song, Hyerim
Hong, Seong Su
Boo, Yong Chool
author_facet Ha, Jae Won
Song, Hyerim
Hong, Seong Su
Boo, Yong Chool
author_sort Ha, Jae Won
collection PubMed
description Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E(2) (PGE(2)) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E(2) synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E(2) synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE(2), and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE(2) production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE(2) production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.
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spelling pubmed-66174192019-07-18 Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter Ha, Jae Won Song, Hyerim Hong, Seong Su Boo, Yong Chool Antioxidants (Basel) Article Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E(2) (PGE(2)) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E(2) synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E(2) synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE(2), and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE(2) production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE(2) production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM. MDPI 2019-06-21 /pmc/articles/PMC6617419/ /pubmed/31234405 http://dx.doi.org/10.3390/antiox8060190 Text en © 2019 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Ha, Jae Won
Song, Hyerim
Hong, Seong Su
Boo, Yong Chool
Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title_full Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title_fullStr Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title_full_unstemmed Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title_short Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E(2) Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter
title_sort marine alga ecklonia cava extract and dieckol attenuate prostaglandin e(2) production in hacat keratinocytes exposed to airborne particulate matter
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6617419/
https://www.ncbi.nlm.nih.gov/pubmed/31234405
http://dx.doi.org/10.3390/antiox8060190
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