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The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin

Oxidative stress-induced cellular senescence and mitochondrial dysfunction result in skin aging by increasing ECM levels-degrading proteins such as MMPs, and decreasing collagen synthesis. MMPs also destroy the basement membrane, which is involved in skin elasticity. The extracellular matrix vitaliz...

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Autores principales: Byun, Kyung-A, Oh, Seyeon, Batsukh, Sosorburam, Kim, Min Jeong, Lee, Je Hyuk, Park, Hyun Jun, Chung, Moon Suk, Son, Kuk Hui, Byun, Kyunghee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044720/
https://www.ncbi.nlm.nih.gov/pubmed/36978943
http://dx.doi.org/10.3390/antiox12030694
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author Byun, Kyung-A
Oh, Seyeon
Batsukh, Sosorburam
Kim, Min Jeong
Lee, Je Hyuk
Park, Hyun Jun
Chung, Moon Suk
Son, Kuk Hui
Byun, Kyunghee
author_facet Byun, Kyung-A
Oh, Seyeon
Batsukh, Sosorburam
Kim, Min Jeong
Lee, Je Hyuk
Park, Hyun Jun
Chung, Moon Suk
Son, Kuk Hui
Byun, Kyunghee
author_sort Byun, Kyung-A
collection PubMed
description Oxidative stress-induced cellular senescence and mitochondrial dysfunction result in skin aging by increasing ECM levels-degrading proteins such as MMPs, and decreasing collagen synthesis. MMPs also destroy the basement membrane, which is involved in skin elasticity. The extracellular matrix vitalizer RA(TM) (RA) contains various antioxidants and sodium hyaluronate, which lead to skin rejuvenation. We evaluated whether RA decreases oxidative stress and mitochondrial dysfunction, eventually increasing skin elasticity in aged animals. Oxidative stress was assessed by assaying NADPH oxidase activity, which is involved in ROS generation, and the expression of SOD, which removes ROS. NADPH oxidase activity was increased in aged skin and decreased by RA injection. SOD expression was decreased in aged skin and increased by RA injection. Damage to mitochondrial DNA and mitochondrial fusion markers was increased in aged skin and decreased by RA. The levels of mitochondrial biogenesis markers and fission markers were decreased in aged skin and increased by RA. The levels of NF-κB/AP-1 and MMP1/2/3/9 were increased in aged skin and decreased by RA. The levels of TGF-β, CTGF, and collagen I/III were decreased in aged skin and increased by RA. The expression of laminin and nidogen and basement membrane density were decreased in aged skin and increased by RA. RA increased collagen fiber accumulation and elasticity in aged skin. In conclusion, RA improves skin rejuvenation by decreasing oxidative stress and mitochondrial dysfunction in aged skin.
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spelling pubmed-100447202023-03-29 The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin Byun, Kyung-A Oh, Seyeon Batsukh, Sosorburam Kim, Min Jeong Lee, Je Hyuk Park, Hyun Jun Chung, Moon Suk Son, Kuk Hui Byun, Kyunghee Antioxidants (Basel) Article Oxidative stress-induced cellular senescence and mitochondrial dysfunction result in skin aging by increasing ECM levels-degrading proteins such as MMPs, and decreasing collagen synthesis. MMPs also destroy the basement membrane, which is involved in skin elasticity. The extracellular matrix vitalizer RA(TM) (RA) contains various antioxidants and sodium hyaluronate, which lead to skin rejuvenation. We evaluated whether RA decreases oxidative stress and mitochondrial dysfunction, eventually increasing skin elasticity in aged animals. Oxidative stress was assessed by assaying NADPH oxidase activity, which is involved in ROS generation, and the expression of SOD, which removes ROS. NADPH oxidase activity was increased in aged skin and decreased by RA injection. SOD expression was decreased in aged skin and increased by RA injection. Damage to mitochondrial DNA and mitochondrial fusion markers was increased in aged skin and decreased by RA. The levels of mitochondrial biogenesis markers and fission markers were decreased in aged skin and increased by RA. The levels of NF-κB/AP-1 and MMP1/2/3/9 were increased in aged skin and decreased by RA. The levels of TGF-β, CTGF, and collagen I/III were decreased in aged skin and increased by RA. The expression of laminin and nidogen and basement membrane density were decreased in aged skin and increased by RA. RA increased collagen fiber accumulation and elasticity in aged skin. In conclusion, RA improves skin rejuvenation by decreasing oxidative stress and mitochondrial dysfunction in aged skin. MDPI 2023-03-11 /pmc/articles/PMC10044720/ /pubmed/36978943 http://dx.doi.org/10.3390/antiox12030694 Text en © 2023 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
Byun, Kyung-A
Oh, Seyeon
Batsukh, Sosorburam
Kim, Min Jeong
Lee, Je Hyuk
Park, Hyun Jun
Chung, Moon Suk
Son, Kuk Hui
Byun, Kyunghee
The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title_full The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title_fullStr The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title_full_unstemmed The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title_short The Extracellular Matrix Vitalizer RA(TM) Increased Skin Elasticity by Modulating Mitochondrial Function in Aged Animal Skin
title_sort extracellular matrix vitalizer ra(tm) increased skin elasticity by modulating mitochondrial function in aged animal skin
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044720/
https://www.ncbi.nlm.nih.gov/pubmed/36978943
http://dx.doi.org/10.3390/antiox12030694
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