Lefaki, MariaPapaevgeniou, NikolettaTur, Josep AVorgias, Constantinos ESykiotis, Gerasimos PChondrogianni, Niki2024-09-132024-09-132020-01Lefaki M, Papaevgeniou N, Tur JA, Vorgias CE, Sykiotis GP, Chondrogianni N. The dietary triterpenoid 18 alpha-Glycyrrhetinic acid protects from MMC-induced genotoxicity through the ERK/Nrf2 pathway. Redox Biol. 2020 Jan;28:101317.2213-2317https://hdl.handle.net/20.500.13003/19854https://hdl.handle.net/20.500.12105/2289018 alpha-Glycyrrhetinic acid (18 alpha-GA) is a bioactive triterpenoid that has been shown to activate the nuclear factor (erythroid-derived-2)-like 2 (Nrf2), the main transcription factor that orchestrates the cellular antioxidant response, in both cellular and organismal context. Although various beneficial properties of 18 alpha-GA have been revealed, including its anti-oxidation and anti-aging activity, its possible protective effect against DNA damage has never been addressed. In this study, we investigated the potential beneficial properties of 18 alpha-GA against DNA damage induced by mitomycin C (MMC) treatment. Using human primary fibroblasts exposed to MMC following pre-treatment with 18 alpha-GA, we reveal an Nrf2-mediated protective effect against MMC-induced cell death that depends on extracellular signal-regulated kinase (ERK) signaling. In total, our results reveal an additional beneficial effect of the Nrf2 activator 18 alpha-GA, suggesting that this important phytochemical compound is a potential candidate in preventive and/or therapeutic schemes against conditions (such as aging) or diseases that are characterized by both oxidative stress and DNA damage.enghttp://creativecommons.org/licenses/by-nc-nd/4.0/18 alpha-Glycyrrhetinic acidNrf2DNA damageMitomycin CERK pathwayPhytochemicalsGlycyrrhetinic AcidOxidative StressApoptosisMAP Kinase Signaling SystemReactive Oxygen SpeciesFibroblastsGene Expression RegulationHumansNF-E2-Related Factor 2DNA DamageCell LineMitomycinThe dietary triterpenoid 18 alpha-Glycyrrhetinic acid protects from MMC-induced genotoxicity through the ERK/Nrf2 pathwayresearch articleAttribution-NonCommercial-NoDerivatives 4.0 International315053262810131710.1016/j.redox.2019.101317Redox Biologyopen accessRegulación de la Expresión GénicaMitomicinaDaño del ADNHumanosFibroblastosEspecies Reactivas de OxígenoEstrés OxidativoApoptosisÁcido GlicirretínicoSistema de Señalización de MAP QuinasasFactor 2 Relacionado con NF-E2Línea Celular2-s2.0-85071869131501490700063L2002834091