The PTEN inhibitor bpV(pic) promotes neuroprotection against amyloid β-peptide (25-35)-induced oxidative stress and neurotoxicity. (3rd August 2017)

• Record Type: Journal Article
• Authors: Liu, Xiao-Ying; Zhang, Li-Jing; Chen, Zhou; Liu, Li-Bin
• Is Part Of: Neurological research. Volume 39:Number 8(2017)
• Page Start: 758
• Page End: 765
• Publication Date: 2017-08-03
• Subjects: Aβ25-35 -- bpV(pic) -- oxidative stress -- neurodegeneration -- neuroprotection; Neurology -- Periodicals; Neurosciences -- Periodicals; 616.8005
• DOI: 10.1080/01616412.2017.1317916
• Languages: English
• ISSNs: 0161-6412

Abstract

Abstract: Objectives : The aim of this study was to elucidate the mechanism underlying the neuroprotective effects of the phosphatase and tensin homolog (PTEN) inhibitor, bisperoxovanadium-pic [bpV(pic)]. Methods: We determined the effects of bpV(pic) on amyloid-β-peptide-(25-35)-induced neurotoxicity, particularly intracellular reactive oxygen species (ROS) production and mitochondria-mediated apoptotic signaling, in a human neuroblastoma (SH-SY5Y) cell model. Results: We found that exposure of SH-SY5Y cells to amyloid β peptides (Aβ25-35 ) resulted in a significant reduction in cell viability accompanied by increased lactate dehydrogenase (LDH) release, elevated levels of intracellular ROS, and decreased superoxide dismutase (SOD) activities, all of which were reversed by co-treatment with bpV(pic). Moreover, bpV(pic) induced significant protection against Aβ25-35 -induced apoptosis, and effectively suppressed mitochondria-dependent apoptotic signaling triggered by Aβ25-35 . Discussion: Aβ peptides are thought to cause neurodegeneration in Alzheimer's disease (AD), via the induction of free radical oxidative stress. Our results indicate that bpV(pic) provides protection against Aβ25-35 -induced oxidative stress and neurotoxicity, suggesting that bpV(pic) could be a potential therapeutic candidate in the treatment of neurodegenerative diseases such as AD.