Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 410, Issue 4, Pages 759-765Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.06.046
Keywords
Hyperoside; Heme oxygenase-1; NF-E2-Related Factor 2; Hydrogen peroxide; Oxidative stress
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Funding
- National Natural Science Foundation [30572366]
- National Science and Technology Major Project [2010ZX09401-306-1-3]
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The flavonoid hyperoside has been reported to elicit cytoprotection against oxidative stress partly by increasing the activity of antioxidant enzymes, such as glutathione peroxidase, superoxide dismutase and catalase. However, the cellular and molecular mechanisms underlying this effect remain unclear. Here, hepatic L02 cells exposed to H2O2 (100 mu M) were used to demonstrate that hyperoside protected cells by significantly inhibiting overproduction of intracellular ROS, depletion of the mitochondrial membrane potential and leakage of lactate dehydrogenase. Hyperoside further enhanced the cellular antioxidant defense system through increasing the activity of heme oxygenase-1 (HO-1), and by up-regulating HO-1 expression. Meanwhile, real time PCR, western blot and immunofluorescence studies revealed that hyperoside stimulated nuclear translocation of the Nrf(2) transcription factor in a dose-dependent manner, and this effect was significantly suppressed by pharmacological inhibition of the mitogen-activated protein kinases (MAPK) p38 and ERK. Collectively, our data provide the first description of the mechanism underlying hyperoside's ability to attenuate H2O2-induced cell damage, namely this compound interacts with the MAPK-dependent Keap(1)-Nrf(2)-ARE signaling pathway to up-regulate HO-1 expression and enhance intracellular antioxidant activity. (C) 2011 Elsevier Inc. All rights reserved.
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