Why the study?
Does Atractylodis macrocephalae rhizoma (AMR) improve ventricular remodeling in rats with isoproterenol-induced myocardial injury?
Does Atractylodis macrocephalae rhizoma (AMR) improve ventricular remodeling in rats with isoproterenol-induced myocardial injury?
Atractylodis macrocephalae rhizoma (AMR) attenuates isoproterenol-induced ventricular remodeling in rats, likely via antioxidative effects and RAAS inhibition.
Myocardial infarction (MI) is the primary cause of ventricular remodeling (VR). The aim of the present study was to determine the effect of Atractylodis macrocephalae rhizoma (AMR) on VR induced by isoproterenol (ISO) in rats. Male Sprague Dawley rats were randomly divided into the normal control, ISO‑induced and AMR groups. Rats in the ISO‑induced and AMR groups were subcutaneously injected with 85 mg/kg/day ISO for two consecutive days. Compared with the ISO‑induced group, AMR normalized the levels of hemodynamic parameters, markedly attenuated myocardial pathological damage, decreased the level of N‑terminal prohormone of brain natriuretic peptide, and inhibited cardiac hypertrophy and myocardial fibrosis. In addition, AMR inhibited oxidative stress and activation of the rennin‑angiotensin‑aldosterone system (RAAS) when compared with the ISO‑induced group. The results of the present study suggest that AMR may reverse VR via its antioxidative effect and inhibition of RAAS activation.
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Cui et al. (2017) studied this question.
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