Inhibition of angiotensin II–induced hypertrophy and cardiac dysfunction by North American ginseng (Panax quinquefolius)

Abstract

We determined whether North American ginseng (Panax quinquefolius L.) mitigates the effect of angiotensin II on hypertrophy and heart failure. Angiotensin II (0.3 mg/kg) was administered to rats for 2 or 4 weeks in the presence or absence of ginseng pretreatment. The effect of ginseng (10 μg/mL) on angiotensin II (100 nM) – induced hypertrophy was also determined in neonatal rat ventricular myocytes. We also determined effects of ginseng on fatty acid and glucose oxidation by measuring gene and protein expression levels of key factors. Angiotensin II treatment for 2 and 4 weeks induced cardiac hypertrophy as evidenced by increased heart weights, as well as the upregulation of the hypertrophy-related fetal gene expression levels, with all effects being abolished by ginseng. Ginseng also reduced abnormalities in left ventricular function as well as the angiotensin II–induced increased blood pressure. In myocytes, ginseng abolished the hypertrophic response to angiotensin II as assessed by surface area and gene expression of molecular markers of hypertrophy. Ginseng modulated angiotensin II–induced abnormalities in gene expression and protein levels of CD36, CPT1M, Glut4, and PDK4 in vivo and in vitro. In conclusion, ginseng suppresses angiotensin II–induced cardiac hypertrophy and dysfunction which is related to normalization of fatty acid and glucose oxidation.