Protection by tetrahydroxystilbene glucoside against neurotoxicity induced by MPP+: the involvement of PI3K/Akt pathway activation.

2011: JChen; XKang; GLi; XLi; YLi; RQin; JSun; LTao;

Toxicol Lett.2011;202(1):1-7.10.1016/j.toxlet.2011.01.001.

NLM PMID: 21237255

Article abstract

Oxidative stress plays an important role in the pathogenesis of Parkinson's disease (PD). 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), which is an active component of the rhizome extract from polygonum multiflorum, shows potent antioxidant properties. In this paper, the neuroprotective effects of TSG on 1-methyl-4-phenylpyridinium (MPP+-induced apoptosis in PC12 cells were investigated. Pretreatment with TSG markedly attenuated MPP+-induced loss of cell viability and release of lactate dehydrogenase (LDH), and reduced MPP+-induced apoptotic cell death in a dose-dependent manner. The anti-apoptotic effects of TSG were probably mediated by the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway since TSG failed to rescue cells from MPP+ injury in the presence of the PI3K inhibitor, LY294002. These results indicate that TSG affords a significant neuroprotective effect against MPP+-induced damage and apoptosis in PC12 cells. The PI3K/Akt signaling pathway might be involved in the TSG-mediated anti-apoptotic effects.

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Last MEDLINE®/PubMed® update: 1st of December 2015