Aim To observe the effect of Salvianolic acid B(SalB) on atherosclerotic plaque stabilization in diabetic atherosclerosis animal models prepared from apolipoprotein E(ApoE) gene knock-out mice treated by intraperitoneal injection of STZ and high fat diet.Methods Fifty two-month female ApoE gene knock-out mice were injected with STZ and fed with high fat diet for 12 weeks.Then fasting blood glucose(FBG) level was measured and forty diabetic atherosclerosis mice were selected for the following treatment experiment.Diabetic atherosclerosis mice were randomly divided into four groups.Each group was fed with same high fat diet and intragastrically administrated with different drugs for 8 weeks,named model group(distilled water),SalB high dose group(160 mg/(kg·d)),SalB medium dose group(80mg/(kg·d)) and Lovastatin group(2.3 mg/(kg·d)).Then frozen sections and paraffin sections of mice aortas were made.The lipid core area,thickness of fibrous cap,incidence of plaque erosion and the number of neovascularization in atheromatous plaque were measured by Sudan III staining,MASSON staining and immunohistochemistry staining. Results Compared with the model group,both the level of FBG and total cholesterol(TC) in the SalB high dose group and Lovastatin group reduced significantly(P<0.05).Compared with the model group,both the level of triglyceride(TG) and low density lipoprotein cholesterol(LDLC) in the SalB medium dose group,SalB high dose group and Lovastatin group reduced significantly(P<0.05),whereas the level of high density lipoprotein cholesterol(HDLC) increased significantly(P<0.05).Compared with the model group,lipid core area,the number of neovascularization in atheromatous plaque and the incidence of plaque erosion in the SalB medium dose group,SalB high dose group reduced significantly(P<0.01),whereas average thickness of fibrous cap became thicker significantly(P<0.01).Conclusions SalB may stabilize the diabetic atherosclerotic plaques by increasing average thickness of fibrous cap and decreasing lipid core area,incidence of plaque erosion and neovascularization in atheromatous plaque.