Quercetin protects neuronal cells from oxidative stress and cognitive degradation induced by amyloid β-peptide treatment.

The present study aimed to investigate the effect of quercetin on cytotoxicity and cognitive degradation induced by amyloid β(Aβ)‑peptide in mice. Using the 1,1-diphenyl-2‑picrylhydrazyl (DPPH) method and a Y‑maze assay, the radical quenching ability and effect on working memory were determined, respectively, of quercetin treatment following 4 days of Aβ administration. The acute oral toxicity was assessed used to determine the concentration of quercetin at which 50% lethality of the neuronal cells was induced. For determination of the effect of quercetin on degradation of learning and memory loss induced by Aβ, a passive avoidance test was used. The results revealed that quercetin was involved in the inhibition of DPPH radical activity and was found to reduce radical activity by 76.5%. Quercetin significantly protected PC12 neuronal cells from death induced by Aβ treatment. Treatment of mice with daily doses of 100 mg/kg body weight quercetin for 30 days significantly improved the degradation of learning and memory loss induced by Aβ. The acute oral dose of quercetin in mice was determined to be 575 mg/kg body weight. Therefore, quercetin was found to be of therapeutic value for the treatment of neurological disorders, including AD, although further investigations are required.