Abstract: AIM To investigate the effect of astragaloside IV on angiogenesis maturity in mice with myocardial infarction(MI) and protein expression of hypoxia-induced factor 1α and vascular endothelial cell factor. METHODS C57BL mice were randomly divided into three groupssham, myocardial infarction(MI model) and astragaloside IV therapy(Astra-MI). MI mice were established by permanent coronary artery ligation. Astragaloside IV(2 mg/kg/day) was administrated intraperitoneally every day for 21 days. Left ventricular ejection fraction and fractional shortening were determined by Animal Visual Sonics System(Canada). Areas at risk and infarct size were determined by Evan's blue and triphenyl tetrazolium chloride(TTC) methods. CD31 and α-SMA fluorescent staining were used to observe the density of angiogenesis and maturity of vessels in the peri-infarction myocardium tissue. Fusion angiogenesis density was determined by FITC-lectin fluorescent staining. Expressions of HIF-1α and VEGF were determined by Western blot. RESULTS Left ventricular ejection fraction and fractional shortening were significantly improved in Astra-MI group, respectively, compared with those in MI model control(61.0±2.7)% vs.(40.2±3.9)%, P<0.05; (44.1±3.2)% vs.(29.1±4.1)%, P<0.05. IS/AAR were significantly attenuated in Astra-MI group(28.8±8.4)% vs.(45.1±9.3)%, P<0. 05. Angiogenesis density, vessel maturity and fusion angiogenesis in peri-infarction myocardium tissues in Astra-MI group were(214.0±21.3)/mm²,(7.0±2.1)/mm², and(0.39±0.11)×10⁴/pixels, respectively, which were all significantly better than those in the control group(P<0.01). Protein expressions of HIF-1α and VEGF in the risk area of MI in Astra-MI group were higher than in controls(P<0.01). CONCLUSION
Astragaloside IV may reduce ischemia injury and improve function by improving effective angiogenesis density in mice with MI. The mechanism of astragaloside IV may be related with increasing HIF-1α and VEGF expressions.