Tetrahydroxystilbene glucoside inhibits α-synuclein aggregation and apoptosis in A53T α-synuclein-transfected cells exposed to MPP
Increasing evidence has solidified the involvement of α-synuclein (α-Syn) and neurotoxins in the pathogenesis of Parkinson’s disease (PD), suggesting a combination of genetic and environmental influences. 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG)
is one of the main active components extracted from Polygonum multiflorum. The purpose of the present study was to investigate the effects of TSG on α-Syn aggregation, mitochondrial dysfunction, oxidative stress, and apoptosis in vitro. A53T mutant α-synuclein-transfected
cells (A53T AS cells) plus MPP+ exposure were used as a complex cell model of PD. The expression of proteins was determined by Western blot assay. Flow cytometry was utilized to measure mitochondrial membrane potential and apoptosis. The results showed that MPP+ exposure
for 24 h induced more severe damage in A53T AS cells than in vector control cells. Pretreatment of TSG for 24 h significantly increased the cell viability; decreased lactate dehydrogenase leakage; inhibited α-Syn over-expression and aggregation; elevated mitochondrial membrane potential;
decreased reactive oxygen species, Bax/Bcl-2 ratio, and caspase-3 activity; and inhibited apoptosis in A53T AS cells exposed to MPP+. These results suggest that TSG may be an attractive candidate for PD therapy.
Keywords: A53T α-synuclein-transfected cell; MPP+; Parkinson’s disease; cellules transfectées avec le gène de l’α-synucléine portant la mutation A53T; maladie de Parkinson; tetrahydroxystilbene glucoside; tétrahydroxystilbène glucoside; α-synuclein; α-synucléine
Document Type: Research Article
Publication date: 01 January 2017
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