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Related Experiment Videos

Ginsenosides Rb1 and Re decrease cardiac contraction in adult rat ventricular myocytes: role of nitric oxide.

G I Scott1, P B Colligan, B H Ren

  • 1Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine, Grand Forks, North Dakota, ND 58203, USA.

British Journal of Pharmacology
|November 13, 2001
PubMed
Summary

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Ginsenosides Rb1 and Re from Panax ginseng directly decrease heart cell contraction. This effect is linked to increased nitric oxide synthase (NOS) activity, suggesting a novel mechanism for ginseng

Area of Science:

  • Cardiovascular Pharmacology
  • Natural Product Chemistry
  • Cellular Physiology

Background:

  • Panax ginseng is traditionally used for stamina and stress relief.
  • Ginsenosides are key bioactive compounds in ginseng, known to influence cardiovascular function.
  • Understanding the cellular mechanisms of ginsenosides is crucial for their therapeutic application.

Purpose of the Study:

  • To investigate the direct effects of ginsenosides Rb1 and Re on cardiac myocyte contractile function.
  • To explore the role of nitric oxide synthase (NOS) in mediating the actions of ginsenosides on cardiomyocytes.

Main Methods:

  • Isolation of adult rat ventricular myocytes.
  • Measurement of contractile properties including peak shortening (PS) and time-to-90% relengthening (TR90).

Related Experiment Videos

  • Assay of nitric oxide synthase (NOS) activity using a 3H-arginine to 3H-citrulline conversion method.
  • Application of ginsenosides Rb1 and Re at varying concentrations (1-1000 nM) and NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME).
  • Main Results:

    • Both ginsenosides Rb1 and Re demonstrated a dose-dependent inhibition of cardiomyocyte peak shortening (PS) and fluorescence intensity change (DeltaFFI), with maximal inhibition around 20-25%.
    • Combined application of Rb1 and Re did not result in additive inhibitory effects on PS.
    • Pretreatment with the NOS inhibitor L-NAME abolished the inhibitory effects of Rb1 and Re on cardiomyocyte contraction.
    • Ginsenosides Rb1 and Re significantly stimulated NOS activity in a concentration-dependent manner (P<0.05).

    Conclusions:

    • Ginsenosides Rb1 and Re exert a direct depressant effect on cardiomyocyte contractility.
    • This negative inotropic effect is, at least partially, mediated by the stimulation of nitric oxide (NO) production via NOS activation.
    • Findings provide cellular evidence for a novel mechanism underlying the cardiovascular effects of Panax ginseng.