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

Li,Yan‑Ling; Guo,Hua; Zhao,Yong‑Qiang; Li,Ai‑Fan; Ren,Yue‑Qin; Zhang,Jie‑Wen

doi:10.3892/mmr.2017.6704

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

Authors:
- Yan‑Ling Li
- Hua Guo
- Yong‑Qiang Zhao
- Ai‑Fan Li
- Yue‑Qin Ren
- Jie‑Wen Zhang
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Affiliations: Department of Neurology, Zhengzhou First People's Hospital, Zhengzhou, Henan 450004, P.R. China, Department of Medicine Imaging, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China, Department of Endocrinology, Anyang District Hospital, Anyang, Henan 455000, P.R. China, Department of Radiology Magnetic Resonance, The Second Affiliated Hospital of Henan Traditional Chinese Medicine University, Zhengzhou, Henan 450000, P.R. China, Department of Neurology, The People's Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China
Published online on: June 6, 2017 https://doi.org/10.3892/mmr.2017.6704
Pages: 1573-1577

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Abstract

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.

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