Genistein Prevents Apoptosis and Oxidative Stress Induced by Methylglyoxal in Endothelial Cells.
Molecules
; 29(8)2024 Apr 10.
Article
em En
| MEDLINE
| ID: mdl-38675531
ABSTRACT
Glycolytic overload promotes accumulation of the highly reactive dicarbonyl compounds, resulting in harmful conditions called dicarbonyl stress. Methylglyoxal (MG) is a highly reactive dicarbonyl species and its accumulation plays a crucial pathophysiological role in diabetes and its vascular complications. MG cytotoxicity is mediated by reactive oxygen species (ROS) generation, a key event underlying the intracellular signaling pathways leading to inflammation and apoptosis. The identification of compounds able to inhibit ROS signaling pathways and counteract the MG-induced toxicity is a crucial step for developing new therapeutic strategies in the treatment of diabetic vascular complications. In this study, the effect of genistein, a natural soybean isoflavone, has been evaluated on MG-induced cytotoxicity in human endothelial cells. Our results show that genistein is able to counteract the MG-induced apoptosis by restraining ROS production, thus inhibiting the MAPK signaling pathways and caspase-3 activation. These findings identify a beneficial role for genistein, providing new insights for its potential clinical applications in preserving endothelial function in diabetic vascular complications.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Aldeído Pirúvico
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Espécies Reativas de Oxigênio
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Apoptose
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Estresse Oxidativo
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Genisteína
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Células Endoteliais
Limite:
Humans
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article