Edaravone inhibits autophagy after neuronal oxygen-glucose deprivation/recovery injury

Edaravone is an oxygen free radical scavenger that is widely used to treat ischemic injury to the nervous system. This study investigated the effect of edaravone pretreatment on neurons subjected to oxygen-glucose deprivation/recovery (OGD/R) injury.Common neurons were subjected to oxygen and glucose deprivation for 1 h, followed by oxygen and glucose recovery for 0.5, 2, 6 and 12 h to establish the OGD/R model. Autophagy was assessed by electron microscope observation of autophagosomes, cell immunofluorescence, mRFP-GFP-LC3 virus cell fluorescence and western blotting analyses of the autophagy-related proteins. The findings showed that at OGD/R 2 h autophagy was high. Next, neurons were pretreated with different concentrations of edaravone (0, 5, 10, 25, 50 and 100 μM) before establishing the OGD/R model. Western blotting was used to analyze the expression of autophagy-related proteins. The CCK-8 assay was used to analyze cell viability after pretreatment with different concentrations of edaravone. Optimal inhibition of autophagy was achieved with the concentration of edaravone 50 μM. Neurons pretreated with 50 μM edaravone and established OGD/R model were analyzed for autophagy levels.At every OGD/R time point autophagy was lower in neurons pretreated with edaravone than in those not pretreated with the drug. The difference was statistically significant without OGD/R 12 h.Pretreatment with edaravone may reduce the level of autophagy in neurons subjected to OGD/R injury.