Abstract
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 H 2O 2-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 H 2O 2-induced neurotoxicity is dependent on increasing SIRT1 and provides a potentially novel pharmacological strategy for stroke prevention and/or treatment. © 2010 The Authors. Basic & Clinical Pharmacology & Toxicology © 2010 Nordic Pharmacological Society.
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CITATION STYLE
Zhang, L., Huang, S., Chen, Y., Wang, Z., Li, E., & Xu, Y. (2010). Icariin inhibits hydrogen peroxide-mediated cytotoxicity by up-regulating sirtuin type 1-dependent catalase and peroxiredoxin. Basic and Clinical Pharmacology and Toxicology, 107(5), 899–905. https://doi.org/10.1111/j.1742-7843.2010.00595.x
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