Hesperidin ameliorates functional and histological outcome and reduces neuroinflammation in experimental stroke

Incidence of stroke is considered to be a major cause of death throughout the world. The middle cerebral artery occlusion (MCAO) for 2 h followed by 22 h of reperfusion model was used in male Wistar rats to study the protection of stroke by hesperidin. Hesperidin administration (50 mg/kg b.wt.) once daily for 15 days has improved the infarct size, reduced the neurological deficits in terms of behaviors, and protected the elevated level of thiobarbituric acid reactive species (TBARS). A significantly depleted activity of antioxidant enzymes, glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) and content of glutathione (GSH) in MCAO group were protected significantly in MCAO group pretreated with hesperidin. Moreover, inflammatory mediators like TNF-α, IL-1β levels, expression of iNOS and glial fibrillary acidic protein (GFAP) were significantly attenuated in H + MCAO group as compared to MCAO group. In conclusion, prophylactic treatment with hesperidin ameliorated the functional and histological outcomes with elevated endogenous antioxidants status as well as reduced induction of proinflammatory cytokines in MCA occluded rat. We theorized that hesperidin is among the pharmacological agents that reduce free radicals and its associated inflammation and have been found to limit the extent of brain damage following stroke.

► MCAO in rats induced neurological deficits and oxidative damage. ► Oxidative stress contributes to the cascade leading to inflammation and neuronal death. ► Hesperidin attenuated cerebral ischemia reperfusion injury in rats.