摘要Far-infrared irradiation exhibits promise in chronic diseases,and its role in ischemic stroke specifically in modulating mitochondrial dynamics remains unknown.This study explored the neuroprotective effects of far-infrared irradiation using a rat middle cerebral artery occlusion model and oxygen-glucose deprivation-injured neuronal cells.In middle cerebral artery occlusion rats,daily 30-minute far-infrared irradiation treatment reduced infarct volume,alleviated cerebral edema,and improved neurological function.Proteomic analysis identified far-infrared irradiation-mediated upregulation of eight proteins,including the mitochondrial fusion regulator optic atrophy 1.In oxygen-glucose deprivation-exposed cells,far-infrared irradiation restored mitochondrial membrane potential,and enhanced fusion via optic atrophy 1 induction.Mechanistically,far-infrared irradiation stabilized mitochondrial dynamics by boosting optic atrophy 1 expression,thereby reducing oxidative stress and maintaining energy production.Optic atrophy 1 knockdown partly abolished the protective effects of far-infrared irradiation therapy.These results establish far-infrared irradiation as a non-pharmacological intervention targeting mitochondrial redox homeostasis in ischemic stroke,offering a novel therapeutic avenue for cerebrovascular disorders.