Download neuroprotective effect of quercetin during hydrogen peroxide

NEUROPROTECTIVE EFFECT OF QUERCETIN AGAINST HYDROGEN PEROXIDEINDUCED CELL DEATH IN THE CULTURE OF P19 NEURONS
Jazvinšćak Jembrek Maja, Pevec Tihana, Erhardt Julija, Oršolić Nada
Oxidative damage by reactive oxygen species (ROS), secondary intermediates in intracellular
signaling, has been implicated in dysfunctions of mammalian brain in numerous diseases and
injuries. The aim of this study was to better understand the molecular mechanisms of
neurodegeneration induced via oxidative stress and the protective effect of flavonoid
quercetin on the neuronal cell death induced by hydrogen peroxide (H2O2) exposure for 24
hours. The effect of quercetin on H2O2-induced injury was investigated in the culture of P19
neurons, differentiated from the P19 mouse embryonal carcinoma cells in the presence of
retinoic acid. Complete neuronal maturation of P19 neurons was confirmed by
immunofluorescence staining against neuron specific marker beta-III tubulin. As determined
by methylthiazolyltetrazolium bromide (MTT) assay, treatment with H2O2 (1.5 mM)
significantly decreased the cell viability. In the dose-dependent manner, quercetin reversed
the toxic effect of H2O2. Release of lactate dehydrogenase (LDH) from H2O2-damaged cell
membranes was also significantly reduced in the presence of quercetin indicating that the P19
neurons were less vulnerable in the presence of quercetin. While H2O2 treatment markedly
induced the production of ROS, increase in cell survival in the presence of quercetin was
accompanied by a significant decrease in ROS production. Quercetin also decreased the
activities of key apoptotic markers caspase-3/7. The obtained results suggest that quercetin,
probably due to the interfering with the apoptotic pathway, can act as survival factor in
neuronal cells. In light of these findings, beneficial effects of quercetin could be taken into
account for potential therapeutic uses in neuroprotection.