Oleocanthal ameliorates amyloid-β oligomers' toxicity on astrocytes and neuronal cells: In vitro studies

Neuroscience. 2017 Jun 3;352:204-215. doi: 10.1016/j.neuroscience.2017.03.059. Epub 2017 Apr 7.

Abstract

Extra-virgin olive oil (EVOO) has several health promoting effects. Evidence have shown that EVOO attenuates the pathology of amyloid-β (Aβ) and improves cognitive function in experimental animal models, suggesting it's potential to protect and reduce the risk of developing Alzheimer's disease (AD). Available studies have linked this beneficial effect to oleocanthal, one of the active components in EVOO. The effect of oleocanthal against AD pathology has been linked to its ability to attenuate Aβ and tau aggregation in vitro, and enhance Aβ clearance from the brains of wild-type and AD transgenic mice in vivo. However, the ability of oleocanthal to alter the toxic effect of Aβ on brain parenchymal cells is unknown. In the current study, we investigated oleocanthal effect on modulating Aβ oligomers (Aβo) pathological events in neurons and astrocytes. Our findings demonstrated oleocanthal prevented Aβo-induced synaptic proteins, SNAP-25 and PSD-95, down-regulation in neurons, and attenuated Aβo-induced inflammation, glutamine transporter (GLT1) and glucose transporter (GLUT1) down-regulation in astrocytes. Aβo-induced inflammation was characterized by interleukin-6 (IL-6) increase and glial fibrillary acidic protein (GFAP) upregulation that were reduced by oleocanthal. In conclusion, this study provides further evidence to support the protective effect of EVOO-derived phenolic secoiridoid oleocanthal against AD pathology.

Keywords: amyloid-β; astrocytes; neuroinflammation; neurons; oleocanthal.

MeSH terms

  • Aldehydes / pharmacology*
  • Amyloid beta-Peptides / toxicity*
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism
  • Anti-Inflammatory Agents / pharmacology*
  • Astrocytes / drug effects*
  • Cell Line, Tumor
  • Cyclopentane Monoterpenes
  • Disks Large Homolog 4 Protein / metabolism
  • Dose-Response Relationship, Drug
  • Glutamate Plasma Membrane Transport Proteins / metabolism
  • Humans
  • Interleukin-6 / metabolism
  • Nerve Tissue Proteins / metabolism
  • Neurons / drug effects*
  • Phenols / pharmacology*
  • Synaptosomal-Associated Protein 25 / metabolism
  • Time Factors
  • Transfection

Substances

  • Aldehydes
  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Anti-Inflammatory Agents
  • Cyclopentane Monoterpenes
  • Disks Large Homolog 4 Protein
  • Glutamate Plasma Membrane Transport Proteins
  • Interleukin-6
  • Nerve Tissue Proteins
  • Phenols
  • SLC1A2 protein, human
  • SNAP25 protein, human
  • Synaptosomal-Associated Protein 25
  • oleocanthal