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Effect of Atractylodes macrocephala rhizoma on isoproterenol‑induced ventricular remodeling in rats
Xiao-Hua Cui1, Hui-Lin Wang1, Rong Wu1
1Department of Pharmacology, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Abstract:
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.
Insights
Atractylodis macrocephalae rhizoma (AMR) may reverse ventricular remodeling after myocardial infarction by reducing oxidative stress and inhibiting the rennin-angiotensin-aldosterone system (RAAS). This study investigated AMR
Area of Science:
- Cardiology
- Pharmacology
- Integrative Medicine
Background:
- Myocardial infarction (MI) is a leading cause of ventricular remodeling (VR).
- Ventricular remodeling significantly impacts cardiac function and patient prognosis.
- Identifying therapeutic agents to mitigate VR is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the effects of Atractylodis macrocephalae rhizoma (AMR) on isoproterenol (ISO)-induced ventricular remodeling in a rat model.
- To elucidate the underlying mechanisms by which AMR may exert protective effects against cardiac damage.
Main Methods:
- Male Sprague Dawley rats were divided into normal control, ISO-induced, and AMR treatment groups.
- Isoproterenol (85 mg/kg/day) was administered subcutaneously for two consecutive days to induce myocardial injury.
- AMR treatment effects were assessed by evaluating hemodynamic parameters, myocardial pathology, cardiac hypertrophy, fibrosis, oxidative stress, and RAAS activation.
Main Results:
- AMR administration normalized hemodynamic parameters compared to the ISO-induced group.
- AMR significantly attenuated myocardial pathological damage, cardiac hypertrophy, and myocardial fibrosis.
- AMR inhibited oxidative stress and suppressed the activation of the rennin-angiotensin-aldosterone system (RAAS).
Conclusions:
- Atractylodis macrocephalae rhizoma (AMR) demonstrates potential in reversing ventricular remodeling induced by isoproterenol.
- AMR's cardioprotective effects are likely mediated through its antioxidant properties and inhibition of RAAS activation.
- AMR may serve as a therapeutic strategy for managing post-myocardial infarction ventricular remodeling.
