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Cardiovascular disease basic research
Effects of Ginsenosides-Rbl inhibiting cardiomyocyte hypertrophy via NHE-1-dependent calcineurin activation ex vivo
  1. Hongliang Kong,
  2. Hongbo Sun,
  3. Lijie Song
  1. Cardiology Center, The People's Hospital Of Liaoning Province, Shenyang, China


Objectives Ginsenosides-Rbl (Gs-Rbl), a main component of Ginsenosides extracted from Ginseng, is a type of activity element playing a therapeutic role in the cardiovascular system. The present study aimed at determining whether Gs-Rbl exerts a direct antihypertrophic effect and the potential underlying mechanisms on cultured cardiomyocytes ex vivo.

Methods Neonatal rat ventricular cardiomyocytes were randomly divided into control group, simple phenylephrine (PE, 5 umol/l, α1 adrenoceptor agonist) group and Gs-Rb1 group (on the basis of PE intervention) for 36 h; The concentration of Gs-Rb1 is 50 umol/l, 100 umol/l, 200 umol/l and 500 umol/l, respectively. Cell surface area, Na+-H+ exchanger 1 (NHE-1), and NFAT3 was analysed.

Results Phenylephrine (PE) leaded to a marked hypertrophic effect on neonatal cardiomyocytes (847±20 m2 to 1147±30 m2, p=0.000); Gs-Rb1 attenuated hypertrophic effect of PE in a concentration-dependent manner (p<0.01), in which ≥200 umol/l Gs-Rb1 exerted a complete inhibition of hypertrophy. PE significantly increased the expression of gene and protein of the NHE-1 (Gene: 1.77±0.08-fold; protein: 1.51±0.04-fold), increased NHE-1 activity (1.61±0.11-fold); Gs-Rb1 inhibited or completely abrogated (≥200 umol/l Gs-Rb1) the above effect of PE in a concentration-dependent manner (p<0.01). NFAT3 was translocated to the nuclei from the cytosol by PE, which was significantly reduced, even similar to control group once the concentration of Gs-Rb1≥100 umol/l, by Gs-Rb1. The effect of PE on increasing calcineurin activity was significantly reduced in the presence of Gs-Rb1, however, which was significantly greater than in control group.

Conclusions Ginsenosides-Rbl inhibited cardiomyocyte hypertrophy induced by phenylephrine ex vivo, which is at least mediated by inhibition of NHE-1-dependent calcineurin pathway.

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