Abstract:Aim To observe the effect of probucol on the atherosclerosis of experimental diabetic rats,and study its related mechanism. Methods Fourty rats were randomly divided into two groups,normal control group and the model group.Streptozotocin(STZ)was injected intraperitoneally to establish experimental diabetic rat models.Twenty-two rats became diabetes successfully and were randomly divided into two groups: diabetes group,probucol treatment group.After 8 weeks,all rats were executed,and the level of blood glucose,serum concentration of HDL,LDL,TC,TG,SOD,MDA,8-iso-PGF2α,platelet endothelial cell adhesion molecule-1(PECAM-1) were tested in each group.The structure of aorta and the thickness of intima was observed by the light microscope,and the expression of PECAM-1in aorta were assayed by immunohistochemistry. Results Compared with the normal control group,the blood glucose,body weight and water consumption of the model group increased significantly(P<0.01).The level of TC,TG and LDL were significantly increased(P<0.01),however HDL decreased.The thickness of intima in the light microscope was in creased(P<0.01),the structure of aorta revealed that intima was added thick and plaque formation mildly.Compared with the diabetes control group,the level of TC and LDL in probucol treatment group decreased significantly(P<0.01),but serum HDL and TG did not change significantly(P>0.05).The thickness of intima in the light microscope decrea sed significantly(P<0.01).Compared with the normal control group,the level of MDA,8-iso-PGF2α and PECAM-1 in diabetes group were significantly increased(P<0.01),but the level of SOD was much lower(P<0.01).Compared with the diabetes group,the level of MDA,8-iso-PGF2α and PECAM-1 in probucol treatment group decreased significantly(P<0.01),and the level of SOD increased significantly(P<0.01).The expression of PECAM-1 in probucol treatment group decreased significantly(P<0.01). Conclusions Probucol treatment can improve the atheromatosis of aorta in experimental diabetic rats.Its protection may be related to anti-oxidant and suppressiont of PECAM-1 expression in diabetic rats.