Background: Ischemic stroke is one of the major causes of mortality and disability worldwide. Limitation of cerebral blood flow due to thrombosis can cause ischemic stroke that in turn affect cellular homeostasis due to insufficient oxygen and nutrient supply. Aims: Reestablishment of cerebral blood flow can cause further deterioration of ischemic brain tissue by a series of inflammatory, apoptotic and oxidative events resulting in cerebral ischemicreperfusion injury which in turn leads to neuronal cell death and neurological impairments. Methods and materials: This study was carried out to evaluate the potential neuroprotective effects of Resatorvid in a global model of cerebral ischemic reperfusion injury in rats. A 24 Wistar-albino rats (weighing 200-300 grams) were divided randomly into 3 groups (n= 8 in each group), a sham (negative control) group, control (ischemic reperfusion group) and Resatorvid group (1mg/kg) intraperitoneally. Rats were exposed to 30 minutes of ischemia followed by 1 hour of reperfusion. At the end of the reperfusion, rats were sacrificed and brain tissue samples were obtained for histopathological scoring and inflammatory markers measuring. Tissue levels of interleukin 1 beta (IL-1b), IL-6, IL-8, and tumor necrosis factor alpha (TNF-a) were significantly lower in Resatorvid pre-treated group as compared to control group (p>0.05) in addition the histopathological score in Resatorvid group were much lower than the control group. Results: we see that administration of Resatorvid can be useful preventive method in attenuating the degree of brain injury during ischemic reperfusion process as shown by a significant reduction of brain inflammatory markers and lower histopathological damage in comparison with control group. Conclusion: the results of the present study revealed that pre-treatment with Resatorvid could confer neuroprotection in global cerebral ischemic reperfusion injury due to it is anti-inflammatory and anti-apoptotic effects.