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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 154279, 10 pages
Research Article

Quercetin Induces Mitochondrial Biogenesis through Activation of HO-1 in HepG2 Cells

1School of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea
2Chitwan Medical College, Bharatpur-10, Chitwan, Nepal
3Korea Bio Medical Science Institute, Seoul 135-818, Republic of Korea
4Graduate School of Oriental Medicine, University of Wonkwang, Iksan 570-300, Republic of Korea
5Department of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA

Received 19 July 2013; Accepted 23 September 2013

Academic Editor: Hong Pyo Kim

Copyright © 2013 Nabin Rayamajhi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The regeneration of mitochondria by regulated biogenesis plays an important homeostatic role in cells and tissues and furthermore may provide an adaptive mechanism in certain diseases such as sepsis. The heme oxygenase (HO-1)/carbon monoxide (CO) system is an inducible cytoprotective mechanism in mammalian cells. Natural antioxidants can provide therapeutic benefit, in part, by inducing the HO-1/CO system. This study focused on the mechanism by which the natural antioxidant quercetin can induce mitochondrial biogenesis in HepG2 cells. We found that quercetin treatment induced expression of mitochondrial biogenesis activators (PGC-1α, NRF-1, TFAM), mitochondrial DNA (mtDNA), and proteins (COX IV) in HepG2 cells. The HO inhibitor SnPP and the CO scavenger hemoglobin reversed the effects of quercetin on mitochondrial biogenesis in HepG2 cells. The stimulatory effects of quercetin on mitochondrial biogenesis could be recapitulated in vivo in liver tissue and antagonized by SnPP. Finally, quercetin conferred an anti-inflammatory effect in the liver of mice treated with LPS and prevented impairment of mitochondrial biogenesis by LPS in vivo. These salutary effects of quercetin in vivo were also antagonized by SnPP. Thus, our results suggest that quercetin enhances mitochondrial biogenesis mainly via the HO-1/CO system in vitro and in vivo. The beneficial effects of quercetin may provide a therapeutic basis in inflammatory diseases and sepsis.