〔Abstract〕 Objective To analyze the effec of dexmedetomidine(Dex) postprocessing in alleviating oxidative stress injury and nuclear factor erythroid 2 related factor 2(Nrf2)/antioxidant response element(ARE) signaling pathways in cerebral ischemia-reperfusion rats. Methods 30 SD rats were randomly divided into sham operation group, model group and Dex group, 10 cases in each group. The modified Longa method was referred to make middle cerebral artery occlusion model in model group and Dex group. The Dex group was intraperitoneally injected with 100 μg/kg Dex(10 mg/L) at immediate reperfusion. After 24 h of reperfusion, The neurological defect score was performed. The cerebral infarction volume was detected by triphenyl tetrazolium chloride(TTC) method. The levels of superoxide dismutase(SOD), malondialdehyde(MDA) and nitric oxide(NO) in brain tissues were determined by ELISA. RT-PCR and Western blot were performed to detect expression of B-cell lymphoma 2(Bcl-2), Bcl-2 associated X protein(Bax), cleaved caspase-3, transcription factor E2 associated factor 2(Nrf2), hemeoxygenase-1(HO-1) and quinone oxidoreductase 1(NQO-1). The brain tissues injury was detected by HE staining and TUNEL staining. Results Compared with sham operation group, neurological defect score score, apoptosis rate, MDA and NO level in model group and Dex group increased(P<0.05), while SOD activity in brain tissue decreased(P<0.05), the expressions of Nrf2, HO-1, NQO-1, cleaved Caspase-3/Bcl-2 and Bax/Bcl-2 were up-regulated(P<0.05). Compared with model group, neurological defect score, cerebral infarction volume, apoptosis rate, MDA and NO level decreased in Dex group(P<0.05), SOD activity in brain tissue increased(P<0.05), and the expressions of Nrf2, HO-1 and NQO-1 were up-regulated(P<0.05), and the expressions of cleaved Caspase-3/Bcl-2 and Bax/Bcl-2 were down-regulated(P<0.05). HE staining showed that pathological changes of brain tissues reduced. Conclusion Dex postprocessing can reduce the oxidative stress injury in CIRI rats, which may be related to the activation of Nrf2/ARE signaling pathway.