Total ginsenosides fought against right ventricular hypertrophy through inhibiting calcineurin signal pathway.
- Author:
Na QIN
;
Li-Wei WEI
;
Xie-Nan HUANG
- Publication Type:Journal Article
- MeSH: Animals; Atrial Natriuretic Factor; Calcineurin; metabolism; Calcineurin Inhibitors; therapeutic use; Ginsenosides; therapeutic use; Heart Ventricles; Hypertrophy, Right Ventricular; drug therapy; metabolism; Male; Monocrotaline; Myocardium; Myocytes, Cardiac; RNA, Messenger; Rats; Rats, Sprague-Dawley; Signal Transduction
- From: Chinese Journal of Integrated Traditional and Western Medicine 2015;35(1):93-97
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of total ginsenosides (TG) on monocrotaline (MCT) induced right ventricular hypertrophy rats, and to explore its correlation with calcineurin (CaN) pathway.
METHODSFifty male Sprague Dawley rats were randomly divided into the normal control group, the MCT model group, and the low, middle, high dose TG treatment groups, 10 in each group. All medication was performed by peritoneal injection for 18 days. Right ventricular peak systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and right ventricular weight/body weight (RVW/BW) were measured. Intracellular free calcium concentrations were measured by Ca2+ fluorescence indicator Fura2/AM. The atrial natriuretic factor (ANF) and CaN mRNA expression of the myocardial tissue were quantitatively analyzed by Real-time PCR. The protein expression of CaN was detected by Western blot.
RESULTSCompared with the MCT model group, preventive treatment of TG at the 3 doses could significantly reduce RVSP, RVHI, RVW/BW, and ANF mRNA expression, and decrease Ca2+ concentration in myocardial cells, CaN mRNA and protein expression in the myocardial tissue.
CONCLUSIONTG could obviously improve MCT-induced right ventricular hypertrophy, which was possibly achieved through suppressing MCT-activated CaN signal transduction.