Objective：To demonstrate the protective effects of edaravone against neuronal anoxia-reoxygenation injury and to investigate the underlying mechanisms. Methods：Acute lucose-oxygen deprivation and subsequent reoxygenation were used to establish anoxia-reoxygenation injury model in cultured hippocampal cells. Cells were treated with different concentrations of edaravone upon reoxygenation. Metabolic rate of MTT, the content of malondialdehyde（MDA） and the activity of NOS were measured by assay kits. The rate of apoptosis was detected by flow cytometry. Results：Edaravone raised the metabolic rate of MTT and reduced malondialdehyde level and activity of NOS of anoxia-reoxygenation injury model in a dose-dependent manner compared with untreated group. The peak of neuroprotective effects occurred at the dose of 100 and 300 -滋mol／L. Cell apoptotic rate was significantly decreased following edaravone treatment（P < 0.01）. There was no significant difference between 100 and 300 -滋mol／L group. Conclusion：Edaravone has protective effect on hippocampal neurons against anoxia-reoxygenation injury by increasing the metabolic rate of MTT, inhibiting lipid peroxidation，reducing the activity of NOS and decreasing apoptosis.