Developing countries have witnessed a considerable surge in stroke incidence. In the wake of effective neuroprotective therapies, natural antioxidants offer a promising area for neuroprotection research. In this context, we investigated the neuroprotective efficacy of linalool (LIN) against transient ischemia (30 min)/reperfusion (7 days) (I/R)-induced brain injury in Wistar albino rats. The oxidative stress enzymatic and non-enzymatic markers were estimated along with behavioral, infarction size, and histopathological evaluations. I/R injury significantly elevated lipid peroxidation (LPO), xanthine oxidase (XO), and nitric oxide (NO), and downregulated protective mechanisms such as superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and total tissue sulfhydryl (T-SH) levels in rat brain. I/R injury produced significant infarction and hippocampal CA1 neuronal death. Further, LIN-treatment, that is, 25, 50, and 100 mg/kg for 1 month (p.o.) significantly enhanced the functional recovery of various neurobehavioral impairments induced by I/R. LIN-treatment also markedly reduced LPO, NO, and XO levels, and significantly improved SOD, CAT, GSH, and T-SH levels. Histopathological and coronal sectioning studies revealed LIN-treatment protected hippocampal CA1 neurons and reduced infarction. The findings of this study indicated that LIN-treatment augmented the antioxidant defense after I/R injury, and showed neuroprotective potential through its antioxidant activity in experimental rats.