The purpose of this research was to explore the molecular mechanisms regarding the beneficial efficacy of EA in the rat model of MCAO/R-induced brain injury, and it was found that EA could prevent neuronal ferroptosis after ischemic stroke by facilitating the Nrf2 nuclear translocation and activating the Nrf2/SLC7A11/GPX4 pathway, which in turn achieves a neuroprotective effect on the nervous system. Here, NFE2L2 is linked to ischemic stroke.