This work was supported by grants AGL2004-302, AGL2007-64042/ALI and project CSD2007-00063 from Programa Consolider-Ingenio from the Spanish Ministry of Science and Innovation (CICYT), and CDTI project number 20060013 with the food company Nutrexpa S.A.
Protection of human HepG2 cells against oxidative stress by the flavonoid epicatechin†
Version of Record online: 29 DEC 2009
Copyright © 2009 John Wiley & Sons, Ltd.
Volume 24, Issue 4, pages 503–509, April 2010
How to Cite
Martín, M. A., Ramos, S., Mateos, R., Izquierdo-Pulido, M., Bravo, L. and Goya, L. (2010), Protection of human HepG2 cells against oxidative stress by the flavonoid epicatechin. Phytother. Res., 24: 503–509. doi: 10.1002/ptr.2961
- Issue online: 24 MAR 2010
- Version of Record online: 29 DEC 2009
- Manuscript Accepted: 6 JUN 2009
- Manuscript Revised: 3 JUN 2009
- Manuscript Received: 21 NOV 2008
- antioxidant defenses;
- biomarkers for oxidative stress;
- cocoa flavonols;
- dietary antioxidants
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.