β-escin activates ALDH and prevents cigarette smoke-induced cell death
Background: The tobacco use is one of the biggest public health threats worldwide. Cigarette smoke contains over 7000 chemicals among other aldehydes, regarded as priority toxicants. β-escin (a mixture of triterpenoid saponins extracted from the Aesculus hippocastanum. L) is a potent activator of al...
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Elsevier
2024-01-01
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Series: | Biomedicine & Pharmacotherapy |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0753332223017225 |
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author | Malwina Sołtysiak Magdalena Paplińska-Goryca Paulina Misiukiewicz-Stępień Paulina Wójtowicz Małgorzata Dutkiewicz Oliwia Zegrocka-Stendel Maria Sikorska Dorota Dymkowska Laura Turos-Korgul Rafał Krenke Katarzyna Koziak |
author_facet | Malwina Sołtysiak Magdalena Paplińska-Goryca Paulina Misiukiewicz-Stępień Paulina Wójtowicz Małgorzata Dutkiewicz Oliwia Zegrocka-Stendel Maria Sikorska Dorota Dymkowska Laura Turos-Korgul Rafał Krenke Katarzyna Koziak |
author_sort | Malwina Sołtysiak |
collection | DOAJ |
description | Background: The tobacco use is one of the biggest public health threats worldwide. Cigarette smoke contains over 7000 chemicals among other aldehydes, regarded as priority toxicants. β-escin (a mixture of triterpenoid saponins extracted from the Aesculus hippocastanum. L) is a potent activator of aldehyde dehydrogenase (ALDH) – an enzyme catalyzing oxidation of aldehydes to non-toxic carboxylic acids. Purpose: The aim of this study was to evaluate the effect of β-escin on ALDH activity, ALDH isoforms mRNA expression and cytotoxicity in nasal epithelial cells exposed to cigarette smoke extract (CSE). Methods: Nasal epithelial cells from healthy non-smokers were treated with β-escin (1 µM) and exposed to 5% CSE. After 6- or 24-hours of stimulation cell viability, DNA damage, ALDH activity and mRNA expression of ALDH isoforms were examined. Results: 24 h β-escin stimulation revised CSE induced cytotoxicity and DNA damage. Cells cultured with β-escin or exposed to CSE responded with strong increase in ALDH activity. This effect was more pronounced in cultures treated with combination of β-escin and CSE. The strongest stimulatory effect on ALDH isoform mRNA expression was observed in cells cultured simultaneously with β-escin and CSE: at 6 h for ALDH1A1 and ALDH3A1, and at 24 h for ALDH1A3, ALDH3A2, ALDH3B1, and ALDH18A1. Combined β-escin and CSE treatment prevented the CSE-induced inhibition of ALDH2 expression at 24 h. Conclusions: β-escin is an effective ALDH stimulatory and cytoprotective agent and might be useful in the prevention or supportive treatment of tobacco smoke-related diseases. |
first_indexed | 2024-03-08T16:33:17Z |
format | Article |
id | doaj.art-78559231a5f84b3e8bcf7802fd9a2d0b |
institution | Directory Open Access Journal |
issn | 0753-3322 |
language | English |
last_indexed | 2024-03-08T16:33:17Z |
publishDate | 2024-01-01 |
publisher | Elsevier |
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series | Biomedicine & Pharmacotherapy |
spelling | doaj.art-78559231a5f84b3e8bcf7802fd9a2d0b2024-01-06T04:37:36ZengElsevierBiomedicine & Pharmacotherapy0753-33222024-01-01170115924β-escin activates ALDH and prevents cigarette smoke-induced cell deathMalwina Sołtysiak0Magdalena Paplińska-Goryca1Paulina Misiukiewicz-Stępień2Paulina Wójtowicz3Małgorzata Dutkiewicz4Oliwia Zegrocka-Stendel5Maria Sikorska6Dorota Dymkowska7Laura Turos-Korgul8Rafał Krenke9Katarzyna Koziak10Department of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, PolandDepartment of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, PolandDepartment of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, PolandDepartment of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, PolandDepartment of Biochemistry and Nutrition, Centre for Preclinical Research and Technology, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, PolandDepartment of Biochemistry and Nutrition, Centre for Preclinical Research and Technology, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, PolandDepartment of Biochemistry and Nutrition, Centre for Preclinical Research and Technology, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, PolandLaboratory of Cellular Metabolism, Nencki Institute of Experimental Biology, Polish Academy of Science, Pasteura 3, 02-093 Warsaw, PolandLaboratory of Cytometry, Nencki Institute of Experimental Biology, Polish Academy of Science, Pasteura 3, 02-093 Warsaw, PolandDepartment of Internal Medicine, Pulmonary Diseases and Allergy, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, PolandDepartment of Biochemistry and Nutrition, Centre for Preclinical Research and Technology, Medical University of Warsaw, Banacha 1b, 02-097 Warsaw, Poland; Corresponding author.Background: The tobacco use is one of the biggest public health threats worldwide. Cigarette smoke contains over 7000 chemicals among other aldehydes, regarded as priority toxicants. β-escin (a mixture of triterpenoid saponins extracted from the Aesculus hippocastanum. L) is a potent activator of aldehyde dehydrogenase (ALDH) – an enzyme catalyzing oxidation of aldehydes to non-toxic carboxylic acids. Purpose: The aim of this study was to evaluate the effect of β-escin on ALDH activity, ALDH isoforms mRNA expression and cytotoxicity in nasal epithelial cells exposed to cigarette smoke extract (CSE). Methods: Nasal epithelial cells from healthy non-smokers were treated with β-escin (1 µM) and exposed to 5% CSE. After 6- or 24-hours of stimulation cell viability, DNA damage, ALDH activity and mRNA expression of ALDH isoforms were examined. Results: 24 h β-escin stimulation revised CSE induced cytotoxicity and DNA damage. Cells cultured with β-escin or exposed to CSE responded with strong increase in ALDH activity. This effect was more pronounced in cultures treated with combination of β-escin and CSE. The strongest stimulatory effect on ALDH isoform mRNA expression was observed in cells cultured simultaneously with β-escin and CSE: at 6 h for ALDH1A1 and ALDH3A1, and at 24 h for ALDH1A3, ALDH3A2, ALDH3B1, and ALDH18A1. Combined β-escin and CSE treatment prevented the CSE-induced inhibition of ALDH2 expression at 24 h. Conclusions: β-escin is an effective ALDH stimulatory and cytoprotective agent and might be useful in the prevention or supportive treatment of tobacco smoke-related diseases.http://www.sciencedirect.com/science/article/pii/S0753332223017225β-escinTobaccoCigarette smoke extractALDHEpithelium |
spellingShingle | Malwina Sołtysiak Magdalena Paplińska-Goryca Paulina Misiukiewicz-Stępień Paulina Wójtowicz Małgorzata Dutkiewicz Oliwia Zegrocka-Stendel Maria Sikorska Dorota Dymkowska Laura Turos-Korgul Rafał Krenke Katarzyna Koziak β-escin activates ALDH and prevents cigarette smoke-induced cell death Biomedicine & Pharmacotherapy β-escin Tobacco Cigarette smoke extract ALDH Epithelium |
title | β-escin activates ALDH and prevents cigarette smoke-induced cell death |
title_full | β-escin activates ALDH and prevents cigarette smoke-induced cell death |
title_fullStr | β-escin activates ALDH and prevents cigarette smoke-induced cell death |
title_full_unstemmed | β-escin activates ALDH and prevents cigarette smoke-induced cell death |
title_short | β-escin activates ALDH and prevents cigarette smoke-induced cell death |
title_sort | β escin activates aldh and prevents cigarette smoke induced cell death |
topic | β-escin Tobacco Cigarette smoke extract ALDH Epithelium |
url | http://www.sciencedirect.com/science/article/pii/S0753332223017225 |
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