This study investigates the effects of electroacupuncture (EA) on ferroptosis in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). EA was found to significantly reduce neurological deficits, cerebral infarct volume, and neuronal damage. EA also decreased iron levels, inhibited lipid peroxidation, increased endogenous antioxidant activity, and modulated the expression of ferroptosis-related proteins. The study further demonstrated that EA promoted nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and increased the expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). However, the protective effects of EA were counteracted by the Nrf2 inhibitor ML385. These findings suggest that EA can suppress ferroptosis and reduce damage caused by cerebral ischemia/reperfusion by activating the Nrf2 signaling axis and increasing the expression of SLC7A11 and GPX4.This study investigates the effects of electroacupuncture (EA) on ferroptosis in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). EA was found to significantly reduce neurological deficits, cerebral infarct volume, and neuronal damage. EA also decreased iron levels, inhibited lipid peroxidation, increased endogenous antioxidant activity, and modulated the expression of ferroptosis-related proteins. The study further demonstrated that EA promoted nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and increased the expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). However, the protective effects of EA were counteracted by the Nrf2 inhibitor ML385. These findings suggest that EA can suppress ferroptosis and reduce damage caused by cerebral ischemia/reperfusion by activating the Nrf2 signaling axis and increasing the expression of SLC7A11 and GPX4.