Attenuation of Aβ toxicity by promotion of mitochondrial fusion in neuroblastoma cells by liquiritigenin

Arch Pharm Res. 2016 Aug;39(8):1137-43. doi: 10.1007/s12272-016-0780-2. Epub 2016 Aug 12.

Abstract

Mitochondrial dynamics control mitochondrial morphology and function, and aberrations in these are associated with various neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. To identify novel regulators of mitochondrial dynamics, we screened a phytochemical library and identified liquiritigenin as a potent inducer of mitochondrial fusion. Treatment with liquiritigenin induced an elongated mitochondrial morphology in SK-N-MC cells. In addition, liquiritigenin rescued mitochondrial fragmentation induced by knockout of mitochondrial fusion mediators such as Mfn1, Mfn2, and Opa1. Furthermore, we found that treatment with liquiritigenin notably inhibited mitochondrial fragmentation and cytotoxicity induced by Aβ in SK-N-MC cells.

Keywords: Amyloid beta; Fusion/fission; Liquiritigenin; Mitochondria dynamics.

MeSH terms

  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Cell Death / drug effects
  • Cell Death / physiology
  • Cell Line, Tumor
  • Flavanones / chemistry
  • Flavanones / pharmacology*
  • Flavanones / therapeutic use
  • Gene Knockout Techniques
  • Humans
  • Mice
  • Mitochondrial Dynamics / drug effects*
  • Mitochondrial Dynamics / physiology
  • Neuroblastoma / drug therapy
  • Neuroblastoma / metabolism*
  • Neuroblastoma / pathology
  • Peptide Fragments / toxicity*

Substances

  • Amyloid beta-Peptides
  • Flavanones
  • Peptide Fragments
  • amyloid beta-protein (1-42)
  • liquiritigenin