Impact of Astragaloside on Ventricular Remodeling and Peroxisome Proliferator Activated Receptor a Expression in Pressure-overload Rats / 中国循环杂志

ABSTRACT

Objective: To study the impact of astragaloside on ventricular remodeling and peroxisome proliferator activated receptor a (PPARa) expression in pressure-overload rats and to preliminarily explore its mechanism. Methods: Pressure-overload rat's model was established by abdominal aorta constriction (AAC) in 8-week old SD rats and the result was conifrmed by echocardiography at 6 weeks later. Pressure-overload rats were divided into 4 groups with different intragastric treatment Model control (normal saline) group, Benazepril hydrochloride [10mg/(kg.d)] group, Low-dose astragaloside [40mg/(kg·d)] group and High-dose astragaloside [80mg/(kg.d)] group; in addition, Sham operation group, the rats received intragastricnormal normal saline.n=20 in each group and all animals were treated for 8 weeks. Rat's cardiac structure and function indexes were assessed by echocardiography, hemodynamic parameter was examined by left ventricular intubation, myocardium and blood levels of free fatty acid (FFA) were determined, morphological changes of myocardial tissue was observed by HE and Masson staining, mRNA and protein expressions of PPARa were measured by qRT-PCR and Western blot analysis. Results: Compared with Sham operation group, Model control group showed increased left ventricular mass index(LVMI), collagen volume fraction (CVF) and FFA level, allP<0.05, while decreased mRNA and protein expressions of PPARa, bothP<0.05. Compared with Model control group, Low-dose and High-dose astragaloside groups presented reduced LVMI, CVF and FFA level, allP<0.05-0.01, while elevated mRNA and protein expressions of PPARa, bothP<0.01. Conclusion:Astragaloside IV mayinhibit myocardial remodeling in pressure-overload rats, which might be via up-regulating mRNA and protein expressions of PPARa, enhance myocardiumFFA utilization, and therefore improve myocardial energy metabolism.