Astragaloside IV inhibits the tumor necrosis factor α-induced cardiomyocyte hypertrophy in neonatal rats

Objective To investigate the protective effects of astragaloside Ⅳ on the tumor necrosis factor α(TNF-α)-induced cardiomyocyte hypertrophy in neonatal rats. Methods Myocardial cells of neonatal rats were cultured in vitro, and hypertrophic cardiomyocytes were induced by TNF-α(25 μmol/L) in the primary cells. The cultured cardiomyocytes from neonatal rats were divided into five groups: normal, TNF-α group and astragaloside Ⅳ treatment groups of 16, 32, 64 μmol/L. The total protein content of cardiomyocytes was determined by Coomassie Brilliant Blue method; the size of cardiomyocytes was measured by digestive isolation and computer photograph analysis system; the cell viability was detected by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetric method; the expression of atrial natriuretic peptide(ANP) mRNA was determined by real-time fluorescent quantitative polymerase chain reaction (RT-PCR); and the secretion of interleukin 1β(IL-1β)in supernatant was determined by enzyme-linked immunosorbent assay (ELISA). ResultsCompared with the normal control group, TNF-α increased the total protein content, cardiomyocoyte size, expression of ANP mRNA, and secretion of IL-1β by 57.3%, 87.5%, 38.3%, 65.4%, respectively, and decreased the cardiomyocyte viability by 48.4% in TNF-α group. Astragaloside Ⅳ of 16, 32, 64 μmol/L could inhibit the TNF-α-induced cardiomyocyte hypertrophy with a dose-dependent relationship. Treatment groups showed that the protein content, cell size, expression of ANP mRNA and secretion of IL-1β decreased, and the cardiomyocyte viability increased. ConclustionAstragaloside Ⅳ could inhibit cardiomyocyte hypertrophy induced by TNF-α in rats, and the mechanism may relate to inflammatory responses.