Aim:To investigate the therapeutic efficacy of quercetin in early brain injury (EBI) and vasospasm resulting from experimental subarachnoid hemorrhage (SAH).Material and Methods:The experimental ratswere assigned to five groups, as follows: Group A rats did not undergo SAH induction; Group B rats underwent SAH induction,but received no treatment; Group C rats underwent SAH induction and received dimethyl sulfoxide (DMSO) intraperitoneally;Group D rats underwent SAH induction, followed by the intraperitoneal administration of 10-mg quercetin;Group E rats underwent SAH induction,followed by the intraperitoneal administration of 50-mg quercetin. After the procedure, each groupof ratsreceived DMSO, 10 mg/kg quercetin, or 50 mg/kg quercetin intraperitoneally at 30 min, 12 h, and 24 h, according to their respective categories. The oxidative stress index (OSI) was biochemically measured usingthe total oxidant status and total antioxidant status. The serum caspase-3, glutathione peroxidase-1 (GPX), and malondialdehyde (MDA) levels were measured. Results:Brain injury and vasospasm after SAH led to a decrease inthe serum GPX levels and an increase in the caspase-3, MDA, and OSI levels. Vasospasm induced an increase in the wall thickness and a narrowing of the lumen diameter in the basilar artery. Treatment with quercetin increasedthe GPX level and decreasedthe caspase-3 and MDA levels. Treatment with quercetin reduced the wall thickness and increasedthe lumen diameter of the basilar artery. Conclusion:Quercetin may be a novel, effective therapeutic option for the treatment of cerebral vasospasm and brain injury by reducing apoptosis, oxidative damage, vessel wall thickness, and vasoconstriction.