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Neuroprotection against hydrogen peroxide-induced toxicity by Dictyophora echinovolvata polysaccharide via inhibiting the mitochondria-dependent apoptotic pathway.
Yu, Wen-Xuan; Lin, Chen-Qiang; Zhao, Qing; Lin, Xin-Jian; Dong, Xiao-Li.
Affiliation
  • Yu WX; Shenzhen Research Institute of The Hong Kong Polytechnic University, State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen, Guangdong, People's Republic of China; Shenzhen Key Laboratory of Food Biological Safety Control, Shenzhen, Guangdong, People's Republic of
  • Lin CQ; Soil and Fertilizer Institute, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian, People's Republic of China.
  • Zhao Q; Department of Neurology, Linzi Maternal & Child Health Hospital of Zibo, Zibo, Shandong, People's Republic of China.
  • Lin XJ; Soil and Fertilizer Institute, Fujian Academy of Agricultural Sciences, Fuzhou, Fujian, People's Republic of China. Electronic address: xinjianlin@163.net.
  • Dong XL; Shenzhen Research Institute of The Hong Kong Polytechnic University, State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen, Guangdong, People's Republic of China; Shenzhen Key Laboratory of Food Biological Safety Control, Shenzhen, Guangdong, People's Republic of
Biomed Pharmacother ; 88: 569-573, 2017 Apr.
Article de En | MEDLINE | ID: mdl-28135600
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 750µM 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. 2h 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.
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Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Polyosides / Basidiomycota / Apoptose / Neuroprotection / Peroxyde d'hydrogène / Mitochondries Limites: Animals Langue: En Journal: Biomed Pharmacother Année: 2017 Type de document: Article

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Polyosides / Basidiomycota / Apoptose / Neuroprotection / Peroxyde d'hydrogène / Mitochondries Limites: Animals Langue: En Journal: Biomed Pharmacother Année: 2017 Type de document: Article
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