Icariin inhibits hydrogen peroxide-mediated cytotoxicity by up-regulating sirtuin type 1-dependent catalase and peroxiredoxin.
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Резюме
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(2) O(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(2) O(2) -induced neurotoxicity is dependent on increasing SIRT1 and provides a potentially novel pharmacological strategy for stroke prevention and/or treatment.