Protective effects of MCI-186 on oxidative damage in a cell model of Alzheimer's disease

被引：5

作者：

Yu, Ming ^{[2
]}

Li, Shujuan ^{[2
]}

Leng, Wenhui ^{[2
]}

Chen, Han ^{[2
]}

Wu, Yingquan ^{[2
]}

Yan, Lirong ^{[1
]}

机构：

[1] Jiangsu Univ, Dept Gerontol, Affiliated Hosp, Zhenjiang 212001, Jiangsu Prov, Peoples R China

[2] Jiangsu Univ, Dept Neurol, Affiliated Hosp, Zhenjiang 212001, Jiangsu Prov, Peoples R China

来源：

NEURAL REGENERATION RESEARCH | 2010年 / 5卷 / 16期

关键词：

MCI-186 (edaravone); oxidative stress damage; beta amyloid protein 25-35; pheochromocytoma (PC12) cells; Alzheimer's disease; neurodegenerative diseases; neural regeneration; GLYCATION END-PRODUCTS; FREE-RADICAL SCAVENGER; AMYLOID-BETA; DNA-DAMAGE; STRESS; MITOCHONDRIAL; EDARAVONE; PROTEIN; SENSITIVITY; HEMORRHAGE;

D O I：

10.3969/j.issn.1673-5374.2010.16.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Oxidative stress has an important role in the development of Alzheimer's disease (AD). Beta amyloid protein 25-35 (A beta(25-35)) can generate oxygen free radicals, and MCI-186 (3-methyl-1-phenyl-2-pyrazolin-5-one, edaravone) can specifically eliminate hydroxyl radicals. The present study introduced A beta(25-35) into PC12 cells to establish a cell model of AD, and investigated the neuroprotective effects of MCI-186 on AD. Results showed that MCI-186 had a positive effect on the prevention and treatment of AD by inhibiting protein oxidative products, advanced glycation end products, lipid oxidative end products and DNA oxidative damage in PC12 cells induced by A beta(25-35).

引用

页码：1226 / 1230

页数：5

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