Ginsenoside F2 possesses anti-obesity activity via binding with PPARγ and inhibiting adipocyte differentiation in the 3T3-L1 cell line

J Enzyme Inhib Med Chem. 2015 Feb;30(1):9-14. doi: 10.3109/14756366.2013.871006. Epub 2014 Mar 25.

Abstract

Abstract Panax ginseng Meyer has been shown to be effective in mitigating various diseases. Protopanaxadiols (PPD) and protopanaxatriols (PPT), which are the main constituents of ginseng, have been shown to impact obesity. Therefore, we selected several important ginsenosides to perform our docking study and determine if they had binding affinity with the peroxisome proliferator activated receptor gamma (PPARγ), which is a major transcription factor in adipocytes. Among them, only a few ginsenosides demonstrated binding affinity with PPARγ. Other than ginsenoside F2 rest of them were previously reported by the researchers in experimental study in case of obesity cell line 3T3-L1 adipocyte. In few recent studies, it was reported that F2 has protective effects on malignant brain tumors as well as anti-cancer activity in breast cancer. Therefore, we felt it was important to focus on F2 when considering obesity. Our study focused on this ginsenoside and analyzed its impact on 3T3-L1 adipocytes. Following the molecular interaction studies, further experimental studies were carried out and demonstrated that ginsenoside F2 when treated with different doses reduces the level of lipid accumulated by the 3T3-L1 cell line during adipogenesis. Reverse transcriptase polymerase chain reaction (RT-PCR) and quantitative real-time PCR results showed reduction in PPARγ and perilipin gene expression levels compared to that of differentiated adipocytes without any treatment. So considering the binding with a major adipocyte transcription factor and the performed experiments, we suggest that ginsenoside F2 may reduce obesity via the inhibition of adipogenesis in the 3T3-L1 cell line.

Keywords: Adipogenesis; PPARγ; Panax ginseng; ginsenoside F2; molecular interaction; obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / cytology
  • Adipocytes / drug effects*
  • Adipocytes / metabolism
  • Adipogenesis / drug effects
  • Adipogenesis / genetics
  • Animals
  • Anti-Obesity Agents / chemistry
  • Anti-Obesity Agents / isolation & purification
  • Anti-Obesity Agents / pharmacology*
  • Binding Sites
  • Carrier Proteins / antagonists & inhibitors*
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Cell Differentiation / drug effects
  • Gene Expression
  • Ginsenosides / chemistry
  • Ginsenosides / isolation & purification
  • Ginsenosides / pharmacology*
  • Humans
  • Lipid Metabolism / drug effects
  • Mice
  • Molecular Docking Simulation
  • PPAR gamma / antagonists & inhibitors*
  • PPAR gamma / chemistry
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Panax / chemistry
  • Perilipin-1
  • Phosphoproteins / antagonists & inhibitors*
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism
  • Plant Extracts / chemistry
  • Protein Binding

Substances

  • Anti-Obesity Agents
  • Carrier Proteins
  • Ginsenosides
  • PPAR gamma
  • Perilipin-1
  • Phosphoproteins
  • Plant Extracts
  • ginsenoside F2