Objective      To investigate the role of ginsenoside-Rg1 in the angiogenesis in rats with acute myocardial ischemia (AMI).       Methods      The acute ischemia model was established by ligation of the left front descending branch of the coronary artery. The rats were divided randomly into the model group

metoprolol treatment (MET

4.5 mg/kg) group

ginsenoside-Rg1 treatment groups (5

10

and 15 mg/kg)

8 rats in each group. Another 8 rats receiving sham operation served as sham operation group. The drugs were administered for 14 d. The myocardial infarction area was measured after 2

3

5-triphenyltetrazoliumchloride (TTC) staining. The microvascular density (MVD) was observed by immunohistochemistry staining. The expression of myocardial VEGF

VEGFR1

VEGFR2 and p-Akt was examined by immunohistochemical staining. The myocardial NO levels were examined by Griess assay.       Results      Compared with the model group

the infarct area was reduced obviously in ginsenoside-Rg1 10 mg/kg group and 15 mg/kg group in AMI rats (P0.01). And also

ginsenoside-Rg1 of 10 and 15 mg/kg resulted in an obvious increase in MVD of ischemic myocardium (P0.01). Ginsenoside-Rg1 of 10 mg/kg led to moderate expression of myocardial VEGF

VEGFR1

VEGFR2 and p-Akt. And that of 15 mg/kg led to strong expression of above proteins. These effects were similar to the positive control group. The best effect was found in the ginsenoside-Rg1 15mg/kg group. In addition

ginsenoside-Rg1 of 10 and 15 mg/kg resulted in an obvious increase in the myocardial NO levels compared with the model group (P0.05

P0.01).       Conclusion      Ginsenoside-Rg1 induces angiogenesis in rats after myocardial ischemia. The role of ginsenoside-Rg1 on angiogenesis is correlated with the increased expression of VEGF

VEGFR

p-Akt and NO in the myocardium.