Purpose:Luteolin recently has been proved to elicit a vanity of biological effects through its antioxidant and antiapoptosis properties.Oxidative and apoptosis damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment.The aim of this study was to evaluate the neuroprotective effects of luteolin and the underlying mechanisms in cerebral ischemia.Methods:Focal cerebral ischemia was induced in adult male Sprague -Dawley rats by permanent middle cerebral artery occlusion (pMCAO).Luteolin was injected intraperitoneally at different doses of 10 0r 25 mg/kg immediately after pMCAO.Experiment l,luteolin s neuroprotective effect was analyzed.Neurological deficits,brain water content and infarct volume were evaluated at 24 and 72 h after pMCAO.SODI,Bcl-2,and Bax expression were measured by immunohistochemistry,western blot and reverse transcription-polymerase chain reaction.Experiment 2,luteolin s anti-oxidative activities were evaluated.SODI,CAT activities,and MDA content were measured by spectrophotometer.Experiment 3,the influence of luteolin on claudin-5 was detected.Results:Compared with MCAO group,luteolin significantly increased the activities of SOD1,CAT,Bcl-2 and claudin-5 (P.05),decreased the levels of MDA and Bax (P.05),and alleviated the neurological deficits,infarct volume and brain water content (P.05).Conducions:The results indicated that luteolin protected the brain from ischemic damage,and this effect may be through reduction of oxidative stress and apoptosis,and upregulation of the expressions of claudin-5.