Aim To observe the influence of ligustrazine on vascular cell adhesion molecule-1(VCAM-1),monocyte chemotactic protein-1(MCP-1) and nuclear factor-κB(NF-κB),expression by vascular endothelial cells and smooth muscle cells and to investigate the molecular mechanism of ligustrazine against atherosclerosis.Methods Human umbilical vein endothelial cells(hUVEC) and rat thorax aortic smooth muscle cells(SMC) were cultured and stimulated by ox-LDL,ox-VLDL,angiotensin Ⅱ and /or ligustrazine.Then,VCAM-1,MCP-1 and NF-κB expression by cultured cells were examed with immunocytochemistry staining or in situ hybridization.Adhesion test of monocytes was used to valuate the influence of ligustrazine on monocytes adhesion to endothelium. Results Comparing with contrast group(hUVEC:0.365±0.019,SMC: 0.416±0.013),ox-LDL,ox-VLDL and angiotensin Ⅱ could inhance VCAM-1 protein level both in hUVEC(0.552±0.008,0.460±0.006,0.486±0.025) and SMC(0.564±0.007,0.513±0.021,0.524±0.008)(p<0.01).As well,ox-LDL,ox-VLDL and angiotensin Ⅱ could inhance MCP-1 protein level both in hUVEC and SMC(p<0.01).By contrast,ox-LDL,ox-VLDL and angiotensin Ⅱ could inhance VCAM-1 and MCP-1 mRNA exprossionS both in hUVEC and SMC(p<0.01).And ligustrazine markedly reduced ox-LDL,ox-VLDL,angiotensin Ⅱ induced VCAM-1 and MCP-1 exprossion(p<0.01).By contrast,ox-LDL,ox-VLDL and angiotensin Ⅱpromoted NF-κB nuclear translocation both in hUVEC and SMC.Ligustrazine inhibited or blocked ox-LDL,ox-VLDL and angiotensin Ⅱ induced NF-κB nuclear translocation.Comparing with ox-LDL,and ox-VLDL group(2.047±0.011,1.936±0.014),ligustrazine reduced the amount of monocytes adhesion to endothelial cells(1.282±0.020,1.265±0.016)(p<0.01). Conclusion Ligustrazine resists atherosclerosis by inhibition of VCAM-1 and MCP-1 expression of vascular cells.This effect might be mediated by NF-κB pathway.