MATERIAL and METHODS: The rats were assigned into 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 and 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 group of rats received DMSO, 10 mg/kg quercetin, or 50 mg/kg quercetin intraperitoneally at 30 minutes, 12 hours, and 24 hours, according to their respective categories. The oxidative stress index (OSI) was biochemically measured using the 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 in the 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 increased the GPX level and decreased the caspase-3 and MDA levels. Treatment with quercetin reduced the wall thickness and increased the 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. Keywords : Early brain injury, Oxidative damage, Quercetin, SAH, Cerebral vasospasm