Aim To assess the effect of atorvastatin on ApoE^-/- mice atherosclerosis and calcification. Methods Six week old male ApoE^-/-mice were fed with diets containing 45% kcal from fat . The mice received diets ad lib for 8 weeks and had free access to water. Then the mice were randomly divided into two groups: atorvastatin group(n6) or high fat group (n6). After 8 weeks of diet, mice were killed，blood was collected and plasma TG,TC,HDL-C,LDL-C,IL-6 and A-SAA concentrations were measured. Aotic sections were stained with hematoxylin and eosin or von kossa and observed under microscope. Immunohistochemical staining was performed to visualize the expresssions of vascular MCP-1,VCAM-1and BMP-2. Human Aorta Endothelial Cells(HAEC) were treated with different doses of atorvastatin. The level of BMP-2,calcium content and AKP activity were measured. Results Serum levels of TG,TC,LDLC,IL-6 and A-SAA in the atorvastatin group significantly decreasd compared with those in the high fat group(P<0.05). Atherosclerotic plaques were observed in ApoE^-/- mice of the high fat group. And the plaque lesions revealed more limited in atorvastatin groups compared with those in the high fat group. However,the calcium mineral deposits on vascular tissue induced by atorvastatin were stronger than the high fat group(P<0.05). The expressions of vascular MCP-1 and VCAM-1 in atorvastatin group significantly decreased compared with those in the high fat group(P<0.01). However,the expression of BMP-2 in atorvastatin group was increased compared with the high fat group(P<0.01). Atorvastatin increased HAECs BMP-2 expression compared with the control group(P<0.05),and further increased the calcium deposition and the activity of AKP significantly compared with the control and low-dose atorvastatin group (P<0.01,P<0.05). Conclusion Atorvastatin may reduce the levels of serum TG,TC,LDLC,IL-6 and A-SAA,decrease the expressions of vascular MCP-1,VCAM-1 and inhibit the progression of atherosclerosis lesion in ApoE^-/- mice. However, Atorvastatin may increase the expression of BMP-2 and accelerate calcium deposition, stimulate the HAEC calcification and the activity of AKP, thus affect calcification of aortic tunica intima.