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 intracellular
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.