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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 490301, 14 pages
Research Article

Ginseng Berry Extract Prevents Atherogenesis via Anti-Inflammatory Action by Upregulating Phase II Gene Expression

1Vascular Homeostasis Laboratory and Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Gangwon-do, Chuncheon 200-701, Republic of Korea
2Department of Surgery, Seoul Medical Center, Seoul 131-130, Republic of Korea
3Amorepacific Corporation R&D Center, Gyeonggi-do, Yongin 446-729, Republic of Korea
4Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Republic of Korea
5Department of Biochemistry, College of Sciences, Yonsei University, Seoul 120-749, Republic of Korea

Received 16 August 2012; Accepted 18 October 2012

Academic Editor: Alvin J. Beitz

Copyright © 2012 Chun-Ki Kim 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.


Ginseng berry possesses higher ginsenoside content than its root, which has been traditionally used in herbal medicine for many human diseases, including atherosclerosis. We here examined the antiatherogenic effects of the Korean ginseng berry extract (KGBE) and investigated its underlying mechanism of action in vitro and in vivo. Administration of KGBE decreased atherosclerotic lesions, which was inversely correlated with the expression levels of phase II genes to include heme oxygenase-1 (HO-1) and glutamine-cysteine ligase (GCL). Furthermore, KGBE administration suppressed NF-κB-mediated expression of atherogenic inflammatory genes (TNF-α, IL-1β, iNOS, COX-2, ICAM-1, and VCAM-1), without altering serum cholesterol levels, in ApoE-/- mice fed a high fat-diet. Treatment with KGBE increased phase II gene expression and suppressed lipopolysaccharide-induced reactive oxygen species production, NF-κB activation, and inflammatory gene expression in primary macrophages. Importantly, these cellular events were blocked by selective inhibitors of HO-1 and GCL. In addition, these inhibitors reversed the suppressive effect of KGBE on TNF-α-mediated induction of ICAM-1 and VCAM-1, resulting in decreased interaction between endothelial cells and monocytes. These results suggest that KGBE ameliorates atherosclerosis by inhibiting NF-κB-mediated expression of atherogenic genes via upregulation of phase II enzymes and thus has therapeutic or preventive potential for atherosclerosis.