Abstract
rhEPO has previously been shown to exert neuroprotective action in focal cerebral ischemia. However, its mechanism is not clear. We established the model of permanent focal cerebral ischemia. rhEPO was administered (5000 IU/kg i.p.) 2 h later after the successful ischemia model in rhEPO group and increased translation of Nrf2 and HO-1 and decreased the H2O2 concentration in the brain confirming activation of the Keap1–Nrf2/ARE pathway. The results show that rhEPO activate Keap1–Nrf2/ARE pathway after ischemia to protect the brain tissue.