ArticleEvidence-based complementary and alternative medicine : eCAM2011
Ginseng (Panax quinquefolius) Reduces Cell Growth, Lipid Acquisition and Increases Adiponectin Expression in 3T3-L1 Cells.
Article in Evidence-based complementary and alternative medicine : eCAM, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- American Ginseng (Nutrients · 2019Review
- Antiobesity Effects of Ginsenoside Rg1 on 3T3-L1 Preadipocytes and High Fat Diet-Induced Obese Mice Mediated by AMPK.Nutrients · 2018Article
- Ginseng and obesity.Journal of ginseng research · 2018Review
- Osteoinduction and proliferation of bone-marrow stromal cells in three-dimensional poly (ε-caprolactone)/ hydroxyapatite/collagen scaffolds.Journal of translational medicine · 2015Article
- Exploring the anti-diabetic potential of Australian Aboriginal and Indian Ayurvedic plant extracts using cell-based assays.BMC complementary and alternative medicine · 2015Article
- American ginseng regulates gene expression to protect against premature ovarian failure in rats.BioMed research international · 2015Article
- Ginsenoside Rg3 reduces lipid accumulation with AMP-Activated Protein Kinase (AMPK) activation in HepG2 cells.International journal of molecular sciences · 2012Article
- A quantified ginseng (Panax ginseng C.A. Meyer) extract influences lipid acquisition and increases adiponectin expression in 3T3-L1 cells.Molecules (Basel, Switzerland) · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (P < .05) in the S phase after 24 and 48 h treatment. Apoptotic cells were modest but significantly (P < .05) increased after 48 h (3.2 ± 1.0%) compared to untreated control cells (1.5 ± 0.1%). Lipid acquisition was significantly reduced (P < .05) 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 (P < .05) 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.
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Registered trials
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