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Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide
Keratinocytes, the major cell type of the epidermis, are particularly sensitive to environmental factors including exposure to sunlight and chemical agents. Since oxidative stress may arise as a result of these factors, compounds are actively sought that can act as protective agents. Recently, canna...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327251/ https://www.ncbi.nlm.nih.gov/pubmed/32863232 http://dx.doi.org/10.1016/j.redox.2020.101613 |
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author | Atalay, S. Dobrzyńska, I. Gęgotek, A. Skrzydlewska, E. |
author_facet | Atalay, S. Dobrzyńska, I. Gęgotek, A. Skrzydlewska, E. |
author_sort | Atalay, S. |
collection | PubMed |
description | Keratinocytes, the major cell type of the epidermis, are particularly sensitive to environmental factors including exposure to sunlight and chemical agents. Since oxidative stress may arise as a result of these factors, compounds are actively sought that can act as protective agents. Recently, cannabidiol (CBD), a phytocannabinoid found in Cannabis Sativa L., has gained increased interest due to its anti-inflammatory and antioxidant properties, and absence of psychoactive effects. This prompted us to analyze the protective effects of CBD on keratinocytes exposed to UVB irradiation and hydrogen peroxide. Here we show, using liquid chromatography mass spectrometry, that CBD was able to penetrate keratinocytes, and accumulated within the cellular membrane. CBD reduced redox balance shift, towards oxidative stress, caused by exposure UVB/hydrogen peroxide, estimated by superoxide anion radical generation and total antioxidant status and consequently lipid peroxidation level. CBD was found to protect keratinocytes by preventing changes in the composition of the cellular membrane, associated with UVB/hydrogen peroxide damages which included reduced polyunsaturated fatty acid levels, increased sialic acid and lipid peroxidation products (malondialdehyde and 8-isoprostanes) levels. This maintains cell membranes integrity and prevents the release of lactate dehydrogenase. In addition, CBD prevented UVB/hydrogen peroxide-induced reduction of keratinocyte size and zeta potential, and also decreased activity of ATP-binding cassette membrane transporters. Together, these findings suggest that CBD could be a potential protective agent for keratinocytes against the harmful effects of irradiation and chemical environmental factors that cause oxidative stress. |
format | Online Article Text |
id | pubmed-7327251 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-73272512020-07-06 Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide Atalay, S. Dobrzyńska, I. Gęgotek, A. Skrzydlewska, E. Redox Biol Research Paper Keratinocytes, the major cell type of the epidermis, are particularly sensitive to environmental factors including exposure to sunlight and chemical agents. Since oxidative stress may arise as a result of these factors, compounds are actively sought that can act as protective agents. Recently, cannabidiol (CBD), a phytocannabinoid found in Cannabis Sativa L., has gained increased interest due to its anti-inflammatory and antioxidant properties, and absence of psychoactive effects. This prompted us to analyze the protective effects of CBD on keratinocytes exposed to UVB irradiation and hydrogen peroxide. Here we show, using liquid chromatography mass spectrometry, that CBD was able to penetrate keratinocytes, and accumulated within the cellular membrane. CBD reduced redox balance shift, towards oxidative stress, caused by exposure UVB/hydrogen peroxide, estimated by superoxide anion radical generation and total antioxidant status and consequently lipid peroxidation level. CBD was found to protect keratinocytes by preventing changes in the composition of the cellular membrane, associated with UVB/hydrogen peroxide damages which included reduced polyunsaturated fatty acid levels, increased sialic acid and lipid peroxidation products (malondialdehyde and 8-isoprostanes) levels. This maintains cell membranes integrity and prevents the release of lactate dehydrogenase. In addition, CBD prevented UVB/hydrogen peroxide-induced reduction of keratinocyte size and zeta potential, and also decreased activity of ATP-binding cassette membrane transporters. Together, these findings suggest that CBD could be a potential protective agent for keratinocytes against the harmful effects of irradiation and chemical environmental factors that cause oxidative stress. Elsevier 2020-06-23 /pmc/articles/PMC7327251/ /pubmed/32863232 http://dx.doi.org/10.1016/j.redox.2020.101613 Text en © 2020 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Research Paper Atalay, S. Dobrzyńska, I. Gęgotek, A. Skrzydlewska, E. Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title | Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title_full | Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title_fullStr | Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title_full_unstemmed | Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title_short | Cannabidiol protects keratinocyte cell membranes following exposure to UVB and hydrogen peroxide |
title_sort | cannabidiol protects keratinocyte cell membranes following exposure to uvb and hydrogen peroxide |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327251/ https://www.ncbi.nlm.nih.gov/pubmed/32863232 http://dx.doi.org/10.1016/j.redox.2020.101613 |
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