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Evidence-Based Complementary and Alternative Medicine
Volume 2011, Article ID 610625, 9 pages
Original Article

Ginseng (Panax quinquefolius) Reduces Cell Growth, Lipid Acquisition and Increases Adiponectin Expression in 3T3-L1 Cells

Department of Chemistry, National University of Singapore, Science Drive 4, Singapore 117543

Received 26 November 2009; Accepted 12 April 2010

Copyright © 2011 Chia-Rou Yeo 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.


An American ginseng (Panax quinquefolius) extract (GE) that contained a quantifiable amount of ginsenosides was investigated for the potential to inhibit proliferation, affect the cell cycle, influence lipid acquisition and adiponectin expression in 3T3-L1 cells. Six fingerprint ginsenosides were quantified by high performance liquid chromatography and the respective molecular weights were confirmed by LC-ESI-MS analysis. The extract contained Rg1 (347.3 ± 99.7 μg g−1, dry weight), Re (8280.4 ± 792.3 μg g−1), Rb1 (1585.8 ± 86.8 μg g−1), Rc (32.9 ± 8 μg g−1), Rb2 (62.6 ± 10.6 μg g−1) and Rd (90.4 ± 3.2 μg g−1). The GE had a dose-dependent effect on 3T3-L1 cell growth, the LC50 value was determined to be 40.3 ± 5 μg ml−1. Cell cycle analysis showed modest changes in the cell cycle. No significant changes observed in both G1 and G2/M phases, however there was a significant decrease in the S phase after 24 and 48 h treatment. Apoptotic cells were modest but significantly increased after 48 h (3.2 ± 1.0%) compared to untreated control cells (1.5 ± 0.1%). Lipid acquisition was significantly reduced by 13 and 22% when treated at concentrations of 20.2 and 40.3 μg ml−1 compared to untreated control cells. In relation to adiponectin activation, western blot analysis showed that the protein expression was significantly increased at concentrations tested. A quantified GE reduced the growth of 3T3-L1 cells, down-regulated the accumulation of lipid and up-regulated the expression of adiponectin in the 3T3-L1 adipocyte cell model.