["Clinical and Experimental Pharmacology and Physiology, Volume 53, Issue 7, July 2026. ", "\nABSTRACT\nFocal cerebral ischemia–reperfusion injury remains a major clinical challenge in stroke management. Electroacupuncture (EA) may confer neuroprotection by modulating key cellular processes; however, its precise role in regulating autophagy‐ferroptosis crosstalk remains largely unclear. The present study aimed to investigate the neuroprotective potential of EA in cerebral ischemia–reperfusion injury, with a focus on exploring potential pathways involving autophagy and ferroptosis regulation. Focal cerebral ischemia–reperfusion injury was modelled using middle cerebral artery occlusion/reperfusion (MCAO/R) in vivo and oxygen–glucose deprivation/reperfusion (OGD/R) in vitro. The therapeutic effect of EA on MCAO/R mice was assessed using several methods, including behavioural tests, cerebral blood flow measurement, and cerebral infarction volume analysis. Molecular analyses used immunofluorescence staining, western blot analysis, and transmission electron microscopy to examine signal transducer and activator of transcription 3 (STAT3)/hypoxia‐inducible factor‐1α (HIF‐1α) pathway activity and its relationship with autophagy/ferroptosis markers. In MCAO/R mice, EA intervention improved neurological functional recovery, decreased cerebral infarction, and enhanced blood flow. EA also downregulated activation of the STAT3/HIF‐1α signalling pathway. Furthermore, EA was associated with reduced markers of excessive autophagy and reduced ferroptosis markers in neurons. IL‐6‐mediated enhancement of STAT3 phosphorylation significantly weakened EA's protective effects against cerebral ischemia–reperfusion injury. In vitro, STAT3 knockdown prevented OGD/R‐induced activation of STAT3/HIF‐1α signalling and was accompanied by reduced autophagy and ferroptosis markers. Our results suggest that EA exerts neuroprotective effects against cerebral ischemic injury, which may be associated with modulation of autophagy and ferroptosis markers via the STAT3/HIF‐1α signalling pathway.\n"]