Please use this identifier to cite or link to this item:
Title: Neuroprotection against hydrogen peroxide-induced toxicity by dictyophora echinovolvata polysaccharide via inhibiting the mitochondria-dependent apoptotic pathway
Authors: Yu, WX
Lin, CQ
Zhao, Q
Lin, XJ
Dong, XL
Keywords: Apoptosis
Oxidative stress
Issue Date: 2017
Publisher: Elsevier Masson
Source: Biomedicine and pharmacotherapy, 2017, v. 88, p. 569-573 How to cite?
Journal: Biomedicine and pharmacotherapy 
Abstract: Neuronal apoptosis caused by toxic stimuli such as oxidative stress is believed to be one of the major reasons in the pathologenesis of neurodegenerative diseases. In the current study, the neuroprotective effects of the crude polysaccharide fraction of edible Dictyophora echinovolvata (DEVP) against H2O2-induced cytotoxicity were investigated using PC12 cells. Following exposure of PC12 cells to 750 μM H2O2, a significant reduction in cell viability and the number of FDA-stained viable neurons as well as an increase in the number of PI-stained dead cells were observed. Furthermore, H2O2 treatment significantly upregulated the protein expression of Bax, cleaved caspases 3 and cytosolic cytochrome c, and down-regulated Bcl-2 levels. 2 h pre-treatment with VP reversed these changes caused by H2O2, including inhibiting neuronal loss and decreasing Bax, cleaved caspases 3 and cytosolic cytochrome c levels, as well as increasing Bcl-2 levels. These results taken together demonstrated that DEVP provided a substantial neuroprotection against H2O2-induced toxicity in PC12 cells, at least partly through inhibiting the mitochondrial apoptotic pathway. These findings suggested that DEVP might be a potential candidate for further preclinical study for preventing neurodegenerative diseases in which oxidative stress and apoptosis are involved.
EISSN: 0753-3322
DOI: 10.1016/j.biopha.2017.01.103
Appears in Collections:Journal/Magazine Article

View full-text via PolyU eLinks SFX Query
Show full item record

Page view(s)

Checked on Sep 18, 2017

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.