Sesaminol glucosides protect beta-amyloid peptide-induced cognitive deficits in mice.

This study was designed to investigate the effect of sesaminol glycosides (SG), one of the most abundant lignan glycosides in sesame (Sesamum indicum LINN.) seed, on cognitive deficits and oxidative stress induced by intracerebroventricular (i.c.v.) injection of beta-amyloid protein (Abeta)(25-35) in mice. Mice were fed diets containing 0%, 0.25%, or 0.5% of SG for six weeks. Dietary SG showed a protective effect against Abeta-induced learning and memory deficits in passive avoidance and the Morris water maze test. Abeta caused significant neuronal loss in the CA1 and CA3 regions of the hippocampus, but SG supplement showed decrease of the Abeta(25-35) induced neuronal loss. The SG supplementation significantly decreased thiobarbituric acid reactive substance values and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in brain tissue. SG also reversed the activity of glutathione peroxidase (GPx), which is decreased by Abeta. These results suggest that SG protects against cognitive deficits induced by Abeta(25-35), in part through its antioxidant activity.