Sodium butyrate exerts antioxidant stress effects and attenuates Aβ25-35-induced cytotoxicity in PC12 cells

Arch Biochem Biophys. 2022 Nov 30:731:109448. doi: 10.1016/j.abb.2022.109448. Epub 2022 Oct 25.

Abstract

Alzheimer's disease (AD), a common neurodegenerative disease, is characterised by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles. An increasing number of studies have demonstrated that Aβ causes neuronal damage and mitochondrial dysfunction. Herein, we evaluated the neuroprotective effect of sodium butyrate (NaB) against Aβ induced neurotoxicity in PC12 cells. The results revealed that 3 mM of NaB promoted the expression of angiotensin-converting enzyme and brain-derived neurotrophic factor, which exert a neuroprotective effect by activating G protein-coupled receptors. Moreover, NaB could significantly improve mitochondrial dysfunction caused by Aβ. In conclusion, NaB protected PC12 cells from Aβ-induced cell damage, highlighting the potential of NaB in AD treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease* / drug therapy
  • Alzheimer Disease* / metabolism
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Peptides / toxicity
  • Animals
  • Antioxidants / metabolism
  • Apoptosis
  • Butyric Acid / pharmacology
  • Cell Survival
  • Membrane Potential, Mitochondrial
  • Neurodegenerative Diseases*
  • Neuroprotective Agents* / pharmacology
  • Neuroprotective Agents* / therapeutic use
  • PC12 Cells
  • Peptide Fragments / metabolism
  • Peptide Fragments / toxicity
  • Rats

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • Butyric Acid
  • Neuroprotective Agents
  • Peptide Fragments