Objective：This study aims to investigate the inhibitory effect of miR-23a-5p on oxidative stress in rats with cerebral ischemia-reperfusion. Methods：The expression of miR-23a-5p in middle cerebral artery occlusion（MCAO） rat model was detected by qPCR assay. MCAO rats were injected with miR-23a-5p lentivirus and 3 groups were seted： Sham group，NC virus group and miR-23a-5p virus group. The nerve damage were evaluated by Berdron score and cerebral infarction volume were evaluated by 2，3，5-triphenyltetrazoliumchloride（TTC）staining. The total superoxide dismutase（SOD）and manganese superoxide dismutase（MnSOD）contents were determined by chemical colorimetry. The contents of 3-nitrotyrosine（3-NT）and nitric oxide（NO）were detected by ELISA. B35 cells，the central nerve cells of rats，were treated with H2O2 to establish oxidative damage mode and 4 groups were seted：control group，miR-23a group，H2O2 group and H2O2+miR-23a group. The total SOD and MnSOD contents were detected by chemical colorimetry，and the contents of 3-NT and NO were detected by ELISA. Results：After ischemia-reperfusion in MCAO rats，the expression of miR-23a-5p decreased rapidly and then gradually increased. In vivo，the overexpression of miR-23a-5p reduced the Berdron score and cerebral infarction volume，decreased the 3-NT and NO levels in serum，increased the total SOD and MnSOD levels. In B35 cells，the overexpression of miR-23a-5p decreased the intracellular levels of 3-NT and NO whereas increased the levels of total SOD and MnSOD. Conclusion：miR-23a-5p can inhibit oxidative damage induced by cerebral ischemia and reperfusion.