OBJECTIVETo investigate the effects and mechanisms of panaxoside Rg1 on the new vessel formation in acute myocardial infarction (AMI) rats.

METHODSThe AMI model of male Sprague-Dawley (SD) rats was established, and rats were randomly divided into the AMI model group, the treatment group of panaxoside Rg1, the placebo group and the treatment group of panaxoside Rg1 plus rapamycin. Cardiac creatases were determined with 1 mL blood drawn from vena caudalis of the rats 48 h after the model was successfully made. After 4 weeks, Evans blue was injected into the aorta roots of the rats, and then, red tetrazoline was dyed again and the myocardial infarction area was evaluated. The microvessel density (MVD) of infarction area was determined by the immunohistochemistry of CD31; enzyme-linked immunosorbent assay (ELISA) was used to detect the protein content of CD31 and hypoxia inducible factor-1alpha (HIF-1alpha) of the infarction area.

RESULTSThe MVD in the infarction area and the contents of CD31 and HIF-1alpha in the Rg1 treatment group were higher than those in the AMI model group significantly (P<0.05). The cardiac creatase and infarction area were lower in the Rg1 treatment group than those in the AMI model group significantly (P<0.05). The above effects, however, disappeared when rapamycin, the antagonist of mammalian target of rapamycin (mTOR), was administered simultaneously.

CONCLUSIONSPanaxoside Rg1 could increase the expression of HIF-1alpha and CD31 of myocardium and stimulate the angiogenesis. The above mentioned role of panaxoside Rg1 might be related to the excitation of mTOR receptor.