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Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 5398542, 11 pages
https://doi.org/10.1155/2017/5398542
Research Article

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

1Research Center of Traditional Chinese Medicine, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
2Department of Pharmacy, Xijing Hospital, Fourth Military Medical University, 169 West Changle Road, Xi’an 710032, China
3Department of Chinese Medicine, Xijing Hospital, Fourth Military Medical University, 169 West Changle Road, Xi’an 710032, China

Correspondence should be addressed to Jianzong Chen; nc.ude.ummf@75nehczj and Jing Ma; nc.ude.ummf@amgnij

Received 26 April 2017; Accepted 25 July 2017; Published 28 September 2017

Academic Editor: Gunhyuk Park

Copyright © 2017 Leitao Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.