文献类型： 外文期刊

作者： Yu, Wen-Xuan ¹ ; Lin, Chen-Qiang ² ; Zhao, Qing ⁵ ; Lin, Xin-Jian ² ; Dong, Xiao-Li ¹ ;

作者机构： 1.Hong Kong Polytech Univ, Shenzhen Res Inst, State Key Lab Chinese Med & Mol Pharmacol Incubat, Shenzhen, Guangdong, Peoples R China

2.Fujian Acad Agr Sci, Soil & Fertilizer Inst, Fuzhou 350003, Fujian, Peoples R China

3.Shenzhen Key Lab Food Biol Safety Control, Shenzhen, Guangdong, Peoples R China

4.Hong Kong Polytech Univ, Dept Appl Biol & Chem Technol, Kowloon, Hong Kong, Peoples R China

5.Linzi Maternal & Child Hlth Hosp Zibo, Dept Neurol, Zibo, Shandong, Peoples R China

关键词： Oxidative stress;Neuroprotection;Apoptosis;Mitochondrial-dependent;Bax;Bcl-2

期刊名称：BIOMEDICINE & PHARMACOTHERAPY （ 影响因子：6.529； 五年影响因子：5.979 ）

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收录情况： SCI

摘要： 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 mM 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 downregulated 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. (C) 2017 Elsevier Masson SAS. All rights reserved.