Article Text

PDF

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

Abstract

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.

Statistics from Altmetric.com

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.