Abstract: Background: Restriction of cerebral blood flow can disturb cellular homeostasis due to insufficient oxygen and nutrient delivery. However, the re-establishment of cerebral blood flow can aggravate the impairment of ischemic brain tissue contributing to a series of oxidative,  inflammatory events resulting in cerebral ischemia-reperfusion (CI/R) injury, which eventually results in neuronal death and neurological disability. Method: An experimental model of 30 Sprague-Dawley rats were randomly allocated to five groups, sham group, I/R group, I/R+(DMSO as a vehicle),I/R+ intraperitoneal (i.p) Empagliflozin 5mg/kg 1 hour before induction of BCCAO, and I/R+intraperitoneal Empagliflozin 10mg/kg 1hour before induction of BCCAO. The brain tissue levels of IL-1β, ICAM-1, and F2-isoprostane were measured in each group in our study. Results: The two doses of (5mg/kg and 10mg/kg) Empagliflozin were significantly reduced the brain tissue level of IL-1β, ICAM-1, and F2-isoprostane as compared to I/R and I/R+vehicle groups.Conclusions: From the results above we concluded that Empagliflozin has a neuroprotective effect seeing that it’s antiinflammatory and anti-oxidant activity.