Study on the Effects of Astragalus Polysaccharides on Heart Function and Myocardial Fibrosis in Sponta-neously Hypertensive Rats and Corresponding Mechanism / 中国药房

ABSTRACT

OBJECTIVE:To investigate the effects of Astragalus polysaccharides on heart function and myocardial fibrosis in spontaneously hypertensive rats (SHR) and corresponding mechanism. METHODS:50 SHR were randomly divided into a model group,a captopril tablets group (positive drug,30 mg/kg) and the groups of high,medium and low-dose (100,50,25 mg/kg) Astragalus polysaccharides,with 10 SHR in each group. Another 10 Wistar Kyoto rats were included into the normal group. The rats in the drug administration groups were given corresponding drugs ip,while those in the normal group and the model group were given isometric distilled water ip,once a day,for 12 consecutive weeks. The left ventricular systolic pressure (LVSP),left ventricular end diastolic pressure (LVEDP),left ventricular pressure rise rate (+dp/dtmax) and left ventricular pressure decline rate (-dp/dtmax) of the rats were recorded. The heart mass index (HMI) and left ventricular mass index (LVMI) thereof were deter-mined. The level of hydroxyproline and the mRNA and protein expression of transforming growth factor-β1(TGF-β1)and peroxi-some proliferator-activated receptor-γ(PPAR-γ)in the cardiac muscle tissue thereof were detected. RESULTS:Compared to the nor-mal group,the rats in the model group had lower LVSP,+dp/dtmax and-dp/dtmax,higher LVEDP,HMI and LVMI,as well as high-er levels of hydroxyproline and the mRNA and protein expression of TGF-β1 and lower level of the mRNA and protein expression of PPAR-γ in the cardiac muscle tissue (P0.05) in all the above-mentioned indexes was shown between the model group and the group of low-dose Astragalus polysaccha-rides,except that the-dp/dtmax of the latter was significantly higher and the level of the mRNA expression of TGF-β1 was obvious-ly lower (P<0.05). CONCLUSIONS:Astragalus polysaccharide can improve heart function and myocardial fibrosis in SHR by a mechanism which may be related to downregulating the expression of TGF-β1 and upregulating the expression of PPAR-γin the car-diac muscle tissue.