Open AccessInhibitory effect of ginsenoside Rb 1 on calcineurin signal pathway in cardiomyocyte hypertrophy induced by prostaglandin F 2α 1
Author(s) -
JIANG Qingsong,
HUANG Xienan,
YANG Guizhong,
JIANG Xiaoyan,
ZHOU Qixin
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00601.x
Subject(s) - atrial natriuretic peptide , medicine , endocrinology , calcineurin , signal transduction , arginine , biology , western blot , nitric oxide , nitric oxide synthase , microbiology and biotechnology , biochemistry , transplantation , amino acid , gene
Aim: To examine the antihypertrophic effect of ginsenoside Rb 1 (Rb 1 ) induced by prostaglandin F 2α (PGF 2α ) in vitro and to investigate the possible mechanisms involved in the calcineurin (CaN) signal transduction pathway. Methods: The cardiomyocyte hypertrophy induced by PGF 2α and the antihypertrophic effect of Rb 1 were evaluated in primary culture by measuring the cell diameter, protein content, and atrial natriuretic peptide (ANP) mRNA expression. ANP and CaN mRNA expressions, CaN and its downstream effectors NFAT 3 and GATA 4 protein expressions, and the intracellular free Ca 2+ concentration ([Ca 2+ ] i ) were assayed by RT‐PCR, Western blot, and fluorescent determination using Fura 2/AM, respectively. Results: PGF 2α (100 nmol/L) significantly increased the cardiomyocyte diameter, protein content and [Ca 2+ ] i , and promoted ANP, CaN mRNA, and CaN/NFAT 3 /GATA 4 protein expressions, which were inhibited by either Rb 1 in a concentration‐dependent manner (50,100, and 200 μg/mL) or L ‐arginine (1 mmol/L). N G ‐nitro‐ L ‐arginine‐methyl ester, a nitric oxide synthase inhibitor, could abolish the effects of L ‐arginine, but failed to change the effects of Rb 1 in the experiments above. Conclusion: The present data implicate that Rb 1 attenuates cardiac hypertrophy, the underlying mechanism may be involved in the inhibition of the Ca 2+ ‐CaN signal transduction pathway.