Aim To observe the expression of Toll like receptor 4(TLR4) and nuclear factor-kappaB(NF-κB) in the model of vascular restenosis established by balloon injury,and the effects of atorvastatin on neoitmal proliferation and expression of TLR4 and NF-κB.To explore a possible role for TLR4/NF-κB pathway in the developing of restenosis. Methods 56 male Sprague-Dawley rats were randomly divided into 5 groups: atorvastatin treatment 1 week group,balloon injury 1 week group,atorvastatin treatment 2 weeks group,balloon injury 2 weeks group,and control group.Balloon catheter denudation of the endothelium in the common carotid artery of the rat was routinely used as a model of restenosis.Immunohistochemistry and reverse transcription-polymerase chain reaction(RT-PCR),Western blot were used to detect the the expression of TLR4 and NF-κB on rat carotid arteries at different groups. Results The proliferation of vascular smooth muscle cell(VSMC) existed on the surface of vascular lumen on 1 week after endothelium denudation.TLR4(15.6%) and NF-κB(9.8%) were stained on SMC of neointimal.The levels of TLR4 mRNA(0.39) and protein(26.18)of carotid arteries were increased compared with those of the control group.After 2 weeks,the neointimal were significantly hyperplasia,the lumen were striking stenosis.Immunostain of TLR4(37.2%) and NF-κB(23.2%)were mostly positive in the neointimal cells.The level of TLR4 mRNA(0.49)and protein((57.12)) of carotid arteries were significantly increased.Treatment of rats with the atorvastatin caused a significant inhibition of the expression of TLR4 and NF-κB as well as neointima form(p<0.05). Conclusion In the model of vascular restenosis by balloon injury,the levels of TLR4 mRNA and protein of carotid arteries were significantly increased and companied with activation of NF-κB.Treatment of rats with the atorvastatin caused a significant inhibition of the expression of TLR4 and NF-κB as well as neointima formation.TLR4 and NF-κB played an important role for TLR4/NF-κB pathway in the developing of restenosis.