Objective To explore the protective effects of edaravone postconditioning on cerebral hypoxiainjury in rats and its effect on the reactive oxygen species (ROS)/thioredoxin interacting protein (TXNIP)/NOD-like receptor-associated protein3 (NLRP3) signaling pathway. Methods Neonatal SD rat cortical neurons were cultured and identified by immunofluorescence staining and randomly divided into 4 groups: neuron group, edaravone group, glucose-oxygen deprivation group, glucose-oxygen deprivation + edaravone group. Neurons in each group were tested for neuronal viability by CCK-8 kit after completion of treatment; neuronal apoptosis by apoptosis kit; neuronal ROS production by ELISA kit; and the expression levels of neuronal proteins by Western blotting. Results The cell viability was significantly decreased after glucose deprivation and hypoxia, and increased significantly after edaravone treatment, and the difference was statistically significant (P＜0.01); after glucose deprivation, the neuronal apoptosis level, ROS content, IL-1β protein expression level, TXNIP protein expression level, IL-18 protein expression level, caspase-1 protein expression level, ASC protein expression level and NLRP3 protein expression level were significantly increased, and decreased significantly after edaravone treatment, and the difference was statistically significant (P＜0.01). Conclusion Edaravone has a neuronal protective effect, which may be related to the inhibition of the ROS/TXNIP/NLRP3 signaling pathway.