http://www.cnr.it/ontology/cnr/individuo/prodotto/ID296001

Neuroprotective Effect of Didymin on Hydrogen Peroxide-Induced Injury in the Neuronal Membrane System (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Neuroprotective Effect of Didymin on Hydrogen Peroxide-Induced Injury in the Neuronal Membrane System (Articolo in rivista) (literal)

Anno

2014-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1159/000365072 (literal)

Alternative label

Morelli, Sabrina; Piscioneri, Antonella; Salerno, Simona; Al-Fageeh, Mohamed B.; Drioli, Enrico; De Bartolo, Loredana (2014)
Neuroprotective Effect of Didymin on Hydrogen Peroxide-Induced Injury in the Neuronal Membrane System
in Cells tissues organs (Print)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Morelli, Sabrina; Piscioneri, Antonella; Salerno, Simona; Al-Fageeh, Mohamed B.; Drioli, Enrico; De Bartolo, Loredana (literal)

Pagina inizio

184 (literal)

Pagina fine

200 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

199 (literal)

Rivista

Cells tissues organs (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

17 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

2-3 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

aInstitute on Membrane Technology, National Research Council of Italy, ITM-CNR, and b Department of Environmental and Chemical Engineering, University of Calabria, Rende , Italy; c National Centre for Biotechnology, King Abdulaziz City for Science and Technology, Riyadh , Saudi Arabia; d WCU Energy Engineering Department, Hanyang University, Seoul , Republic of Korea (literal)

Titolo

Neuroprotective Effect of Didymin on Hydrogen Peroxide-Induced Injury in the Neuronal Membrane System (literal)

Abstract

In this study, the flavonoid didymin was administered in vitro in neuronal cells after hydrogen peroxide (H2O2)-induced injury (neurorescue) in order to investigate the effects of this natural molecule on cell damage in a neuronal membrane system. The results showed the effects of didymin in neuronal cells by using a polycaprolactone biodegradable membrane system as an in vitro model. Two major findings are presented in this study: first is the antioxidant property of didymin and, second, for the first time we provide evidence concerning its ability to rescue neuronal cells from oxidative damage. Didymin showed radical scavenging activities and it protected the neuronal cells against H2O2-induced neurotoxicity. Didymin increased cell viability, decreased intracel-lular reactive oxygen species generation, stimulated superoxide dismutase, catalase and glutathione peroxidase activity in neuronal cells which were previously insulted with H2O2. In addition, didymin strikingly inhibited H2O2-induced mitochondrial dysfunctions in terms of reduction of mitochondria membrane potential and the activation of cleaved caspase-3, and also decreased dramatically the H2O2-induced phosphorylation of c-Jun N-terminal kinase. Therefore, this molecule is capable of inducing recovery from oxidative damage, and promoting and/or restoring normal cellular conditions. Moreover, the mechanism underlying the protective effects of didymin in H2O2-injured neuronal cells might be related to the activation of antioxidant defense enzymes as well as to the inhibition of apoptotic features, such as p-JNK and caspase-3 activation. These data suggest that didymin may be a potential therapeutic molecule for the treatment of neurodegenerative disorders associated with oxidative stress. (C) 2014 S. Karger AG, Basel (literal)

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