Delphinidin ameliorates beta-amyloid-induced neurotoxicity by inhibiting calcium influx and tau hyperphosphorylation

Biosci Biotechnol Biochem. 2009 Jul;73(7):1685-9. doi: 10.1271/bbb.90032. Epub 2009 Jul 7.

Abstract

Beta-amyloid (Abeta) has been suggested to induce neurotoxicity in Alzheimer's disease. We evaluated the neuroprotective effects of delphinidin, an anthocyanidin commonly present in pigmented fruits and vegetables, against Abeta-induced toxicity. Abeta (25-35) significantly decreased the viability of PC12 cells, and this was accompanied by an increase in intracellular calcium levels and tau phosphorylation. However, treatment with delphinidin rescued PC12 cells from Abeta by attenuating the elevation of intracellular calcium levels and tau phosphorylation. Taken together, these results suggest that delphinidin protects PC12 cells against Abeta-induced toxicity by attenuating intracellular calcium influx and tau hyperphosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / antagonists & inhibitors*
  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Anthocyanins / pharmacology*
  • Calcium / metabolism*
  • Calcium Signaling / drug effects*
  • Cell Survival / drug effects
  • Intracellular Space / drug effects
  • Intracellular Space / metabolism
  • Neuroprotective Agents / pharmacology*
  • PC12 Cells
  • Phosphorylation / drug effects
  • Rats
  • tau Proteins / metabolism*

Substances

  • Amyloid beta-Peptides
  • Anthocyanins
  • Neuroprotective Agents
  • tau Proteins
  • delphinidin
  • Calcium