To evaluate the mechanism of vascular endothelial growth factor (VEGF) on the prevention of restenosis after angioplasty, the recombinant adenovirus vector containing hVEGF16s cDNA was constructed and transfected into vascular smooth muscle cells (VSMC) in vitro. The conditioned medium containing VEGF was collected 72 h after the infection. Then, the VSMC and human umbilical vein endothelial cells (HUVEC) were divided into control group, H202-treated group and H202+ VEGF-treated group to observe the proliferation and apoptosis by water soluble tetrazolium (WST-1)method, in situ nick end labeling (TUNEL) and flow cytometry(FCM). Compared with the control and H202+VEGF-treated groups, the absorbance (A) value of HUVEC was decreased, and apoptosis of HUVEC was significantly increased in H202-treated group. The changes of A value and apoptosis of VSMC were contrary to those of HUVEC. H202 could stimulate the proliferation of VSMC and induce the apoptosis of HUVEC, inhibit the proliferation of HUVEC and the apoptosis of VSMC and induce restenosis. VEGF could inhibit the effect of H202on HUVEC and VSMC and prevent restenosis. These results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.