Neuroprotective Effects of Gigantol on Cerebral Ischemia–Reperfusion Injury in Rats via Regulation of Inflammation, Oxidative Stress, and Apoptotic Mechanisms

Background Cerebral ischemic stroke, a devastating neurological condition, arises from the disruption of blood flow to the brain, resulting in oxygen and nutrient deprivation and subsequent neuronal damage. Ischemic stroke is responsible for a significant number of all stroke incidences, highlighting the urgency for effective treatments. Purpose The present study aimed to investigate the therapeutic efficacy of gigantol in rats with cerebral ischemia–reperfusion injury (CI–RI). Materials and Methods The CI–RI was induced in experimental rats, and gigantol was administered intragastrically at 10 and 20 mg/kg concentrations for 7 days prior to CI–RI induction and for an additional 14 days. The levels of brain edema and infarction in the experimental rats were assessed. The concentrations of antioxidants, oxidative stress markers, inflammatory cytokines, and apoptotic proteins were assessed using the kits. Results The current findings demonstrated that gigantol treatment significantly reduced brain edema and infarction levels in CI–RI-induced rats. The gigantol treatment considerably reduced pro-inflammatory cytokine levels and alleviated oxidative stress by enhancing antioxidant concentrations in the brains of CI–RI rats. The gigantol treatment also regulated the levels of apoptotic proteins in the rats with CI–RI. Conclusion The current study revealed the neuroprotective effects of gigantol in rats subjected to CI–RI due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. These findings may promote the advancement of gigantol as a potential salutary candidate to treat brain damage due to ischemic stroke.