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Hyperoside attenuates hydrogen peroxide-induced L02 cell damage via MAPK-dependent Keap₁-Nrf₂-ARE signaling pathway.

Authors :
Xing HY
Liu Y
Chen JH
Sun FJ
Shi HQ
Xia PY
Source :
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2011 Jul 15; Vol. 410 (4), pp. 759-65. Date of Electronic Publication: 2011 Jun 13.
Publication Year :
2011

Abstract

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 H(2)O(2) (100 μM) 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 H(2)O(2)-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.<br /> (Copyright © 2011 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1090-2104
Volume :
410
Issue :
4
Database :
MEDLINE
Journal :
Biochemical and biophysical research communications
Publication Type :
Academic Journal
Accession number :
21689633
Full Text :
https://doi.org/10.1016/j.bbrc.2011.06.046