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

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.

Author information

1
a Graduate School, Beijing University of Chinese Medicine , Beijing 100029 , China.
2
b Laboratory of Academician, Experimental Research Center , China Academy of Chinese Medical Sciences , Beijing 100700 , China.
3
c Shanghai University of Traditional Chinese Medicine , Shanghai 201203 , China.

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

PMID:
28696167
DOI:
10.1080/10286020.2017.1339349
[Indexed for MEDLINE]

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