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Protection of human HepG2 cells against oxidative stress by the flavonoid epicatechin
Author(s) -
Martín María Angeles,
Ramos Sonia,
Mateos Raquel,
IzquierdoPulido María,
Bravo Laura,
Goya Luis
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2961
Subject(s) - oxidative stress , glutathione , reactive oxygen species , glutathione reductase , glutathione peroxidase , malondialdehyde , lactate dehydrogenase , chemistry , antioxidant , flavonoid , biochemistry , pharmacology , viability assay , cell , biology , superoxide dismutase , enzyme
Flavanols, such as epicatechin (EC), constitute an important part of the human diet; they can be found in green tea, grapes and cocoa and possess different biological activities such as antioxidant, anti‐inflammatory and anticarcinogenic. This study investigated the potential chemo‐protective effect of EC against oxidative stress induced by tert‐butylhydroperoxide (t‐BOOH) on human HepG2 cells. Cell viability by lactate dehydrogenase assay and markers of oxidative status: reduced glutathione (GSH), malondialdehyde (MDA), reactive oxygen species (ROS), glutathione peroxidase (GPx) and glutathione reductase (GR) were evaluated. Pretreatment of cells with EC for 20 h prevented the enhanced cell damage and GPx and GR activities as well as the decrease in GSH induced by t‐BOOH. The increased ROS generation induced by t‐BOOH was also partly prevented by a pretreatment for 20 h with EC. In addition, pretreatment of cells with EC for 20 h recovered the t‐BOOH‐induced MDA concentration to control values. A pretreatment for 2 h with EC did not reduce cell damage but partly recovered GSH, reduced ROS levels and muffled the increase of GPx and GR after exposure to t‐BOOH. Treatment of HepG2 cells with concentrations of EC in the micromolar range confers a significant protection against oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd.