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作 者:Ming Yu Shujuan Li Wenhui Leng Han Chen Yingquan Wu Lirong Yan
机构地区:[1]Department of Neurology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China [2]Department of Gerontology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China
出 处:《Neural Regeneration Research》2010年第16期1226-1230,共5页中国神经再生研究(英文版)
基 金:the Talent Introduction Project of Affili-ated Hospital of Jiangsu University,No.jdfyRC 2008003
摘 要:Oxidative stress has an important role in the development of Alzheimer's disease (AD). Beta amyloid protein 25-35 (Aβ25-35) can generate oxygen free radicals, and MCI-186 (3-methyl-l-phenyl-2-pyrazolin-5-one, edaravone) can specifically eliminate hydroxyl radicals. The present study introduced Aβ25-35 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 Aβ25-35.Oxidative stress has an important role in the development of Alzheimer's disease (AD). Beta amyloid protein 25-35 (Aβ25-35) can generate oxygen free radicals, and MCI-186 (3-methyl-l-phenyl-2-pyrazolin-5-one, edaravone) can specifically eliminate hydroxyl radicals. The present study introduced Aβ25-35 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 Aβ25-35.
关 键 词:MCI-186 (edaravone) oxidative stress damage beta amyloid protein 25-35 pheochromocytoma (PC12) cells Alzheimer's disease neurodegenerative diseases neural regeneration
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