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.