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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 7927568, 9 pages
https://doi.org/10.1155/2018/7927568
Research Article

Tetrahydroxystilbene Glucoside Produces Neuroprotection against 6-OHDA-Induced Dopamine Neurotoxicity

Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China

Correspondence should be addressed to Feng Zhang; moc.361@cmzgnefgnahz

Received 16 March 2017; Revised 7 July 2017; Accepted 11 December 2017; Published 14 January 2018

Academic Editor: Fakhrul Islam

Copyright © 2018 Chun Huang 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) was one of the most common neurodegenerative diseases with a slow and progressive loss of dopamine (DA) neurons in the midbrain substantia nigra (SN). Neuroinflammation was identified to be an important contributor to PD pathogenesis with the hallmark of microglia activation. Tetrahydroxystilbene glucoside (TSG) was the main active component extracted from Polygonum multiflorum and held amounts of pharmacological activities including antioxidant, free radical-scavenging, anti-inflammation, and cardioprotective properties. Recent studies demonstrated that TSG exerted neuroprotection from several neurodegenerative disease models. However, the underlying mechanisms were not completely elucidated. In the present study, rat nigral stereotaxic injection of 6-hydroxydopamine- (6-OHDA-) elicited DA neuronal injury was performed to investigate TSG-mediated neuroprotection on DA neurons. In addition, primary rat midbrain neuron-glia cocultures were applied to explore the mechanisms underlying TSG-exerted neuroprotection. Results showed that daily intraperitoneal injection of TSG for 14 consecutive days significantly protected DA neurons from 6-OHDA-induced neurotoxicity and suppressed microglia activation. Similar neuroprotection was shown in primary neuron-glia cocultures. In vitro studies further demonstrated that TSG inhibited microglia activation and subsequent release of proinflammatory factors. Moreover, TSG-mediated neuroprotection was closely related with the inactivation of mitogen-activated protein kinase (MAPK) signaling pathway. Together, TSG protects DA neurons from 6-OHDA-induced neurotoxicity via the inhibition of microglia-elicited neuroinflammation. These findings suggest that TSG might hold potential therapeutic effects on PD.