Neuroprotective effect of α-mangostin on mitochondrial dysfunction and α-synuclein aggregation in rotenone-induced model of Parkinson's disease in differentiated SH-SY5Y cells

J Asian Nat Prod Res. 2017 Aug;19(8):833-845. doi: 10.1080/10286020.2017.1339349.

Abstract

The study was designed to evaluate the protective effect of α-mangostin and explore its mechanism in an in vitro model of Parkinson's disease (PD) induced by rotenone. SH-SY5Y cells were treated with rotenone and α-mangostin for 24 h. α-Mangostin significantly and concentration-dependently inhibited rotenone-induced cytotoxicity. The rotenone-induced aggregation of α-synuclein and loss of TH were alleviated by α-mangostin. α-Mangostin treatment also reversed the rotenone-induced overproduction of reactive oxygen species, activation of caspases (-8 and -3) and mitochondrial dysfunction, reflected by decrease in mitochondrial membrane potential and cellular ATP levels. These findings suggest that α-mangostin has neuroprotective effects against PD-related neuronal injury.

Keywords: Parkinson’s disease; mitochondrial dysfunction; rotenone; α-Mangostin; α-synuclein.

MeSH terms

  • Apoptosis / drug effects
  • Autophagy / drug effects
  • Cell Survival / drug effects
  • Dose-Response Relationship, Drug
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Molecular Structure
  • Neuroprotective Agents / pharmacology*
  • Parkinson Disease / drug therapy*
  • Reactive Oxygen Species / pharmacology
  • Rotenone / pharmacology*
  • Xanthones / chemistry
  • alpha-Synuclein / pharmacology

Substances

  • Neuroprotective Agents
  • Reactive Oxygen Species
  • Xanthones
  • alpha-Synuclein
  • Rotenone
  • mangostin