Βeta-sitosterol enhances motor coordination, attenuates memory loss and demyelination in a vanadium-induced model of experimental neurotoxicity.

Environmental discharge of vanadium causes cognitive and behavioral impairments in humans and animals via production of reactive oxygen species leading to lipid peroxidation and alteration in antioxidant defence system. The current study was carried out to investigate the cognitive-enhancing ability of β-sitosterol in vanadium-induced neurotoxicity. Forty eight mice were randomly assigned into 4 groups (A-D) with the following treatments: group A; distilled water, B; α-tocopherol + sodium metavanadate (NaO3V), C; β-sitosterol + NaO3V and D; only NaO3V. NaO3V was administered intraperitoneally while other treatments were administered through gavage for 7 consecutive days. Neurobehavioral parameters measuring cognition, locomotion, anxiety and grip strength were evaluated at day 8. Following sacrifice, brain levels of catalase, superoxide dismutase, glutathione, malonaldehyde (MDA) and hydrogen peroxide (H2O2) were measured. Immunohistochemical expression of Myelin Basic Protein (MBP) in the brain was also investigated. The results showed that deficits in spatial learning, locomotor efficiency, and motor coordination, induced by acute vanadium neurotoxicity were mitigated by beta-sitosterol. Significantly (α ≤ 0.05) decreased in vivo antioxidant enzyme activities, increased brain levels of MDA and H2O2, structural damage to myelin sheaths and decreased expression of MBP were also observed in the NaO3V group (D), however, co-administration of β-sitosterol reduced these pathologic features. It is concluded that β-sitosterol alleviates vanadium-induced neurotoxicity by enhancing cognition and improving motor co-ordination via its antioxidant and myelo-protective activities.