AimTo establish the rabbit model of atherosclerotic vulnerable plaques, and study the effects of prostaglandin E1 on the angiogenesis which is induced by atherosclerosis.Methed30 New Zealand white rabbits were randomly divided into 3 groups (model group, prostaglandin E1 group, and simvastatin group), each group has 10 rabbits.The rabbit model of atherosclerotic vulnerable plaques were established, and the rabbits were given drugs to affect the disease.The abdominal aorta were processed and examined by hematoxylin-eosin (HE) staining.The angiogenesis and hemorrhage in plaques was detected.The vulnerability index was counted.Immunohistochemical staining was performed to detect the expressions of related factors.And the reverse transcription polymerase chain reaction (RT-PCR) was done to observe the expression of hypoxia-inducible factor-1α (HIF-1α) mRNA and vascular endothelial growth factor (VEGF) mRNA.ResultsCompared with the model group, the expression levels of vulnerability index and platelet-endothelial cell adhesion molecule-1 (CD31) in the prostaglandin E1 group were less (1.23±0.20 vs 2.84±0.59, p<0.05; 1.23±0.20 vs 2.84± 0.59, p<0.05).The expression levels of HIF-1α, VEGF were lower in plaques (0.252±0.032 vs 0.439±0.044, p<0.01; 0.396±0.026 vs 0.673±0.084, p<0.01).The expression levels of HIF-1α mRNA and VEGF mRNA were lower in plaques too (0.706±0.030 vs 1.183±0.134, p<0.05; 0.121±0.019 vs 0.468±0.022, p<0.05).However, the expression levels of HIF-1α and HIF-1α mRNA between the prostaglandin E1 group and simvastatin group are different (0.252±0.032 vs 0.163±0.018, p<0.05; 0.706±0.030 vs 0.763±0.018, p<0.05).ConclusionProstaglandin E1 inhibits angiogenesis of atherosclerotic vulnerable plaque, and it works by reducing the expression of HIF-1α and VEGF.