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

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:

• α-Mangostin
• Parkinson’s disease
• mitochondrial dysfunction
• α-synuclein
• rotenone

Acknowledgments

The authors wish to thank Prof. Chun-Ling Zhang from the Institute of Biophysics, Chinese Academy of Science, for critical reading of the paper.