Objective To clarify the effect of edaravone-regulated nuclear factor kappa-B (NF-κB) signaling pathway on hypoxia-induced cerebral vascular endothelial cell injury.Methods Rat cerebral vascular endothelial cells were isolated and divided into Control, Model (hypoxia treatment), Edaravone-10 μmol/L (hypoxia and 10 μmol/L edaravone treatment), Edaravone-20 μmol/L (hypoxia and 20 μmol/L edaravone treatment), Edaravone-40 μmol/L (hypoxia and 40 μmol/L edaravone treatment), Edaravone-40 μmol/L+PMA (hypoxia and 40 μmol/L edaravone, NF-κB signal activator PMA treatment) group. Methyl thiazolyl tetrazolium (MTT) method was used to detect changes in cell proliferation activity in each group; flow cytometry was used to analyze changes in cell apoptosis; the kits were used to detect levels of reactive oxygen species (ROS), malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); Western blot method was used to detect the expression of cysteine aspartic protease (Caspase)-3, cleaved cysteine aspartic protease (C-Caspase)-3, Caspase-9 and C-Caspase-9 and p65 protein.Results Compared with the Control group, the apoptosis level of cerebral vascular endothelial cells in the Model group increased, the cell proliferation activity decreased, the expression levels of C-Caspase-3, C-Caspase-9, p65, ROS, MDA and LDH were increased, the expression levels of Caspase-3, Caspase-9, SOD and GSH-Px were decreased. Compared with the Model group, in the Edaravone-10 μmol/L, Edaravone-20 μmol/L, Edaravone-40 μmol/L groups, the apoptosis level of cerebral vascular endothelial cells gradually decreased, and the cell proliferation activity gradually increased, the expression levels of C-Caspase-3, C-Caspase-9, p65, ROS, MDA and LDH gradually decreased, the expression levels of Caspase-3, Caspase-9, SOD and GSH-Px gradually increased. Compared with the Edaravone-40 μmol/L group, in the Edaravone-40 μmol/L+PMA group, the proliferation activity of cerebral vascular endothelial cells was reduced, the apoptosis rate was increased, and the expression of C-Caspase-3, C-Caspase-9, p65, ROS, MDA and LDH were increased, the expression of Caspase-3, Caspase-9, SOD and GSH-Px were decreased.Conclusion Edaravone reduces hypoxia-induced cerebral vascular endothelial cell damage by inhibiting NF-κB signaling.