Aim To investigate the influence of lipopolysaccharide (LPS)-induced adventitial inflammation on artery in timal proliferation and its mechanism. Methods 24 New Zealand rabbits were fed with high cholesterol diet for 2 weeks, two sides of iliac artery were randomly divided into two groups: LPS group ( n = 24) and control group ( n = 24). A nonconstrictive polyethylene cuff was placed loosely around the iliac artery of New Zealand rabbits, between the artery and the cuff, and a sterilized cotton thread was placed, which was previously soaked overnight in 6 mg/L LPS in saline. Animals were killed at intervals of 0 day ( n = 8) ,3 days { n = 8), 2 weeks ( n = 8) after surgery. The morphology of the artery and the immunochemistory expression of nuclear factor (NF) κB p65 in the artery was investigated. Results In LPS group, 3 days after surgery, inflammation cells migrated into artery from both the luminal and adventitial side, and 2 weeks after surgery, inflammation cells could only be seen in adventitia; NFκB p65 was expressed in endothelium and adventitial cell in LPS group 3 days after surgery; 2 weeks after surgery, LPS group have increasd intimal area (0.93 ± 0.14 mm2), compared with control group(0.75 ± 0.15 mm2) (P< 0.05). Conclusions LPS-induced adventitial inflammation contributes to intimal proliferation, and the activation of NFκB in endothelium and adventital cells may be the mechanism of it.