Objective: The proliferation and migration of vascular smooth muscle cells (VSMC) are the pathological basis of atherosclerotic formation and vascular restenosis after percutaneous transluminal coronary angioplasty (PTCA) The purpose of this research was to injure the vascular intima, mimicking the formation process of atherosclerosis and PTCA and to observe the effect of c myc antisense RNA on preventing atherosclerotic formation and vascular restenosis Methods: The femur artery intima of 36 male Japanese white rabbits was injured by balloon sac and at the same time, either c myc antisense RNA or sense RNA (1 mg per rabbit) or saline was injected into the blood All the rabbits were fed with hypercholesterol feed and killed in 12 weeks The femur artery was cut into 4 μm thick paraffin sections and stained for PCNA, actin and CD 34 by s p immunohistochemistry The thickness of the intima was measured and the percentage of PCNA positive cells was counted by image analysis (LUZX) Results: In the control group of sense RNA and saline, the intima became much thicker (317 μm), the formation of atherosclerotic plaque was obvious and the number of PCNA positive cells in the intima and the media significantly increased The proliferating cells in the intima were actin positive and the endothelial cells were CD 34 positive But in the antisense RNA group, the thickness of the intima is only half of that of control group (217 μm) and the number of PCNA positive cells (30 5%) were significantly lower than that of the control group (63%) Conclusion: c myc antisense RNA could significantly inhibit the proliferation of VSMC and attenuated the development of atherosclerotic plaque and could be used to prevent the formation of atherosclerosis and vascular restenosis Objective: The proliferation and migration of vascular smooth muscle cells (VSMCs) the pathological basis of atherosclerotic formation and vascular restenosis after percutaneous transluminal coronary angioplasty (PTCA) The purpose of this research was to injure the vascular intima, mimicking the formation process of atherosclerosis and PTCA and observe the effect of c myc antisense RNA on preventing atherosclerotic formation and vascular restenosis Methods: The femur artery intima of 36 male Japanese white rabbits was injured by balloon sac and at the same time, either c myc antisense RNA or sense RNA (1 mg per rabbit) or saline was injected into the blood All the rabbits were fed with hypercholesterol feed and killed in 12 weeks The femur artery was cut into 4 μm thick paraffin sections and stained for PCNA, actin and CD 34 by sp immunohistochemistry The thickness of the intima was measured and the percentage of PCNA positive cells was counted by image anal Results: In the control group of sense RNA and saline, the intima was much thicker (317 μm), the formation of atherosclerotic plaque was obvious and the number of PCNA positive cells in the intima and the media significantly increased The proliferating cells in the intima were actin positive and the endothelial cells were CD 34 positive But in the antisense RNA group, the thickness of the intima is only half of that of control group (217 μm) and the number of PCNA positive cells (30 5% ) were significantly lower than that of the control group (63%) Conclusion: c myc antisense RNA could significantly inhibit the proliferation of VSMC and attenuated the development of atherosclerotic plaque and could be used to prevent the formation of atherosclerosis and vascular restenosis