Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5560258 | Food and Chemical Toxicology | 2017 | 14 Pages |
â¢2â²-O-galloylhyperin prevented CCl4-induced liver injury.â¢2â²-O-galloylhyperin protects against H2O2-induced cell death via inhibition of ROS generation and cellular apoptosis.â¢2â²-O-galloylhyperin inhibited H2O2-induced MAPK activation.â¢AKT activation mediates 2â²-O-galloylhyperin induced Nrf2/HO-1 activation and cytoprotection.
2â²-O-galloylhyperin (2â²-O-GH), an active compound isolated from Pyrola calliantha, possesses remarkable antioxidant activity. The aims of this study were to investigate the hepatoprotective effect of 2â²-O-GH against oxidative stress and elucidate the underlying mechanistic signaling pathways in HepG2 cells as well as in an animal model. Results showed that 2â²-O-GH significantly inhibited hydrogen peroxide (H2O2)-induced HepG2 cell death in a dose dependent manner. The mitogen-activated protein kinase activation, ROS production, mitochondrial membrane potential, intracellular calcium level and subsequent apoptotic protein activation in H2O2-stimulated HepG2 cells were remarkably inhibited by 2â²-O-GH. Furthermore, 2â²-O-GH stimulation resulted in a fast and dramatic activation of Akt and nuclear translocation of the NF-E2-related factor 2 (Nrf2), along with the increased expression of heme oxygenase-1 (HO-1) and levels of glutathione (GSH). Meanwhile, histopathological evaluation of the liver also revealed that 2â²-O-GH effectively ameliorated CCl4-induced the hepatic damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Therefore, these results suggested the hepatoprotective effect of 2â²-O-GH might be correlated with its antioxidant and free radical scavenger effect.
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