Protective effect of erythropoietin on β-amyloid-induced PC12 cell death through antioxidant mechanisms

被引：92

作者：

Li, Gang ^{[2
]}

Ma, Rong ^{[1
]}

Huang, Chengfang ^{[2
]}

Tang, Qiang ^{[1
]}

Fu, Qin ^{[1
]}

Liu, Hui ^{[1
]}

Hu, Benrong ^{[1
]}

Xiang, Jizhou ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Pharmacol, Wuhan 430030, Peoples R China

[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Neurol, Wuhan 430022, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2008年 / 442卷 / 02期

关键词：

erythropoietin; A beta; PC12; cells; apoptosis; oxidative stress;

D O I：

10.1016/j.neulet.2008.07.007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Erythropoietin (EPO), a haematopoietic growth factor has been reported to display neuroprotective properties in different animal models. In the present study, we investigated the neuroprotective effects of EPO on A beta(25-35)-induced neuronal toxicity and its potential mechanisms in PC12 cells. A beta(25-35) significantly reduced cell viability and increased the number of apoptotic-like cells. In addition, increased ROS production and decreased mitochondrial membrane potential were also found after A beta(25-35) exposure. All of these phenotypes induced by A beta(25-35) were markedly reversed by EPO. Pretreatment with EPO prior to A beta(25-35) exposure significantly elevated cell viability, reduced A beta(25-35)-induced apoptosis, decreased ROS production, and stabilized mitochondrial membrane potential. Furthermore, EPO also attenuated the downstream cascade following ROS, including Bcl-2/Bax, and caspase-3 activation. Our results suggest that EPO holds potential for neuroprotection and therefore, may be promising for the treatment of Alzheimer's disease. (c) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：143 / 147

页数：5

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