Icariin Inhibits Hydrogen Peroxide-Mediated Cytotoxicity by Up-regulating Sirtuin Type 1-Dependent Catalase and Peroxiredoxin

被引:35
|
作者
Zhang, Ling [1 ]
Huang, Siyuan [1 ]
Chen, Yanting [1 ]
Wang, Zhongyuan [1 ,2 ]
Li, Erguang [1 ,2 ,3 ]
Xu, Yun [1 ,2 ,3 ]
机构
[1] Nanjing Univ, Dept Neurol, Affiliated Drum Tower Hosp, Sch Med, Nanjing 210008, Jiangsu Prov, Peoples R China
[2] Jiangsu Key Lab Mol Med, Jiangsu, Peoples R China
[3] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Nanjing 210008, Jiangsu Prov, Peoples R China
关键词
ALZHEIMERS-DISEASE BRAIN; CELL-SURVIVAL; LIPID-PEROXIDATION; FREE-RADICALS; DAMAGE; ACTIVATION; ANTIOXIDANTS; MECHANISM; NEURONS; P53;
D O I
10.1111/j.1742-7843.2010.00595.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Previous studies suggest that flavonol icariin protects against neuron injury after oxygen and glucose deprivation by increasing SIRT1. This study demonstrates that icariin can inhibit H2O2-induced neurotoxicity. The neuroprotection of icariin enhances the antioxidant capacity through both a direct scavenging effect on over-produced free radicals and an indirect stimulating effect on the expression and activity of cellular antioxidant enzymes including catalase (CAT) and peroxiredoxin 1 (Prx1). The mechanism may be partially involved in the up-regulation of SIRT1. The SIRT1 antagonist can partly block this neuroprotection and the enhancement of CAT/Prx1 by icariin. These results indicate that the effect of icariin on H2O2-induced neurotoxicity is dependent on increasing SIRT1 and provides a potentially novel pharmacological strategy for stroke prevention and/or treatment.
引用
收藏
页码:899 / 905
页数:7
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