Cyanidin 3-O-glucopyranoside protects and rescues SH-SY5Y cells against amyloid-beta peptide-induced toxicity

Neuroreport. 2008 Oct 8;19(15):1483-6. doi: 10.1097/WNR.0b013e32830fe4b8.

Abstract

The amyloid-beta (A beta) peptide (1-42) aggregation into oligomeric and fibrillar species affects neuronal viability, having a causal role in the development of Alzheimer's disease. Among dietary anthocyanins, cyanidin 3-O-glucoside (Cy-3G) and its metabolites, such as protocatechuic acid (PA), have gained attention as potential neuroprotective agents. In this in-vitro study, we demonstrated that Cy-3G, but not PA, can inhibit A beta1-42 spontaneous aggregation using thioflavin T fluorescence assay and transmission electron microscopy. Furthermore, treatment of human neuronal SH-SY5Y cells with Cy-3G during oligomeric and fibrillar A beta1-42 treatment prevents neuronal viability loss. These protective effects were still evident when Cy-3G treatment was initiated after the appearance of oligomeric A beta1-42 neurotoxicity. Taken together, these results suggest that Cy-3G may protect and rescue the neuronal cells from toxicity induced by A beta1-42.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / chemistry
  • Amyloid beta-Peptides / toxicity*
  • Anthocyanins / pharmacology*
  • Apoptosis / drug effects*
  • Benzothiazoles
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Drug Evaluation, Preclinical / methods
  • Glucosides / pharmacology*
  • Humans
  • Microscopy, Electron, Transmission
  • Microscopy, Fluorescence / methods
  • Neurons / drug effects*
  • Neurons / pathology
  • Neurons / ultrastructure
  • Neuroprotective Agents / pharmacology
  • Peptide Fragments / toxicity
  • Thiazoles / chemistry

Substances

  • Amyloid beta-Peptides
  • Anthocyanins
  • Benzothiazoles
  • Glucosides
  • Neuroprotective Agents
  • Peptide Fragments
  • Thiazoles
  • cyanidin-3-O-beta-glucopyranoside
  • thioflavin T