期刊文献+

Protective effects of MCI-186 on oxidative damage in a cell model of Alzheimer's disease 被引量:5

Protective effects of MCI-186 on oxidative damage in a cell model of Alzheimer’s disease
下载PDF
导出
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.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 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
关键词 MCI-186 (edaravone) oxidative stress damage beta amyloid protein 25-35 pheochromocytoma (PC12) cells Alzheimer's disease neurodegenerative diseases neural regeneration MCI-186 (edaravone) oxidative stress damage beta amyloid protein 25-35 pheochromocytoma (PC12) cells Alzheimer's disease neurodegenerative diseases neural regeneration
  • 相关文献

参考文献1

二级参考文献9

  • 1施婵宏,李剑伟.依达拉奉治疗重型颅脑损伤的疗效分析[J].江苏医药,2005,31(12):925-926. 被引量:8
  • 2Pimplikar SW. Reassessing the amyloid cascade hypothesis of Alzheimer's disease[J]. Int J Bioehem Cell Biol, 2009, 41 (6) : 1261-1268.
  • 3Niyaz M, Numakawa T, Matsuki Y, et al. MCI 186 prevents brain tissue from neuronal damage in cerebral infarction through the aetivation of intracellular signaling[J].J Neurosei Res, 2007,85 (13):2933-2942.
  • 4Pensalfini A, Ceechi C, Zampagni M, et al. Protective effect of new S-acylglutathione derivatives against amyloid-induced oxidative stress[J]. Free Radic Biol Med, 2008,44(8): 1624 1636.
  • 5Pratic D. Evidence of oxidative stress in Alzheimer's disease brain and antioxidant therapy:lights and shadows[J]. Ann N Y AcadSci,2008,1147:70- 78.
  • 6Lee HG,Zhu X,Castellani RJ, et al. Amyloid beta in Alzheimer disease: the null versus the alternate hypotheses[J]. J Pharmacol Exp Ther, 2007,321 (3) : 823-829.
  • 7Sonnen JA, Breimer JC, Lovell MA, et al. Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models[J]. Free Radie Biol Med,2008,45(3):219-230.
  • 8Rudolph E. Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspeetive[J]. Cell, 2005,120 (2) : 545- 555.
  • 9Otani H,Togashi H,Jesmin S,et al. Temporal effects of edaravone,a free radical scavenger, on transient ischemia-induced neuronal dysfunction in the rat hippocampus[J]. Eur J Pharmacol, 2005,512(2 3) : 129 137.

共引文献4

同被引文献18

引证文献5

二级引证文献34

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部