Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
β-escin activates ALDH and prevents cigarette smoke-induced cell death.
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Sołtysiak Malwina, Paplińska-Goryca Magdalena, Misiukiewicz-Stępień Paulina, Wójtowicz Paulina, Dutkiewicz Małgorzata, Zegrocka-Stendel Oliwia, Sikorska Maria, Dymkowska Dorota, Turos-Korgul Laura, Krenke Rafał, Koziak Katarzyna
Аннотация
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.
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.