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Ginsenoside Rf, a component of ginseng, regulates lipoprotein metabolism through peroxisome proliferator-activated

Hyunghee Lee1, Frank J Gonzalez, Michung Yoon

  • 1Department of Life Sciences, Mokwon University, Taejon 302-729, Republic of Korea.

Biochemical and Biophysical Research Communications
|November 22, 2005
PubMed
Summary
This summary is machine-generated.

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Ginseng, particularly ginsenoside Rf, influences lipoprotein metabolism by interacting with peroxisome proliferator-activated receptor alpha (PPARalpha). This effect was observed in wild-type mice but not in PPARalpha-null models, confirming PPARalpha

Area of Science:

  • Biochemistry
  • Pharmacology
  • Metabolic Research

Background:

  • Lipoprotein metabolism is crucial for cardiovascular health.
  • Peroxisome proliferator-activated receptor alpha (PPARalpha) plays a key role in regulating lipid metabolism.
  • Ginseng is a traditional herbal medicine with various bioactive compounds.

Purpose of the Study:

  • To investigate the role of ginseng in regulating lipoprotein metabolism.
  • To determine if ginseng's effects are mediated through peroxisome proliferator-activated receptor alpha (PPARalpha) pathways.
  • To identify specific ginseng components responsible for these effects.

Main Methods:

  • Utilized a peroxisome proliferator-activated receptor alpha (PPARalpha)-null mouse model.
  • Administered ginseng extract, ginsenosides, and specific ginsenosides (like Rf) to wild-type and PPARalpha-null mice.

Related Experiment Videos

  • Measured hepatic apolipoprotein (apo) A-I and C-III mRNA levels.
  • Assessed PPARalpha reporter gene expression.
  • Investigated the mechanism of action of ginsenoside Rf on PPARalpha activity.

    • Main Results:

    • Ginseng extract, ginsenosides, and ginsenoside Rf increased basal hepatic apo A-I and C-III mRNA levels in wild-type mice.
    • These ginseng components reversed the reduction of apo A-I and C-III mRNA induced by a PPARalpha ligand (Wy14,643) in wild-type mice.
    • No effects were observed in PPARalpha-null mice, indicating a PPARalpha-dependent mechanism.
    • Ginsenoside Rf was identified as the primary active component responsible for ginseng's effects on lipoprotein metabolism.
    • Ginsenoside Rf appears to inhibit PPARalpha-dependent transactivation by interfering with DNA binding.

    Conclusions:

    • Ginseng component ginsenoside Rf regulates apolipoprotein A-I and C-III mRNA levels.
    • The effects of ginsenoside Rf on lipoprotein metabolism are mediated through interactions with peroxisome proliferator-activated receptor alpha (PPARalpha).
    • Ginseng may represent a potential therapeutic agent for modulating lipoprotein metabolism via PPARalpha pathways.