Salidroside Protects against MPP+-Induced Neuronal Injury through DJ-1-Nrf2 Antioxidant Pathway

Abstract EN

Parkinson’s disease (PD) is the second most common neurodegenerative disorder.

We have found that salidroside (Sal) exhibited neuroprotective effects against MPP+ toxicity.

However, the molecular mechanism is not fully understood.

In this study, we found that Sal significantly prevented MPP+-induced decrease of mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in SH-SY5Y cells.

Moreover, silencing of Nrf2 significantly inhibited Sal-induced increase in mRNA and protein expression of GCLc, SOD1, and SOD2.

But Nrf2 silence did not significantly impact Sal-exhibited effects on DJ-1 expression.

Silencing of Nrf2 significantly suppressed the decrease of apoptosis induced by Sal in MPP+-treated SH-SY5Y cells.

Sal significantly prevented MPP+-induced decrease of the mRNA and protein expression of DJ-1 in SH-SY5Y cells.

Moreover, silencing of DJ-1 significantly inhibited Sal-induced increase in mRNA and protein expression of Nrf2, GCLc, SOD1, and SOD2 in MPP+-treated SH-SY5Y cells.

These results indicated that DJ-1 was an upstream regulator of Nrf2 in the neuroprotective effects of Sal.

Furthermore, silencing of DJ-1 significantly suppressed the decrease of apoptosis induced by Sal in MPP+-treated SH-SY5Y cells.

In conclusion, Sal prevented MPP+-induced neurotoxicity through upregulation of DJ-1-Nrf2-antioxidant pathway.

Our findings provide novel insights into the neuroprotective effects of Sal against PD.