Aim To investigate the relationship between advanced glycosylation end products (AGEs) and the changes of extracellular matrix (ECM) of aorta in diabetic rats in the development of atherosclerosis. Methods Wistar rats were divided into three groups: induced diabetic rats (DM group), aminoguanidine (AG) treated diabetic rats (AG group) and the control rats (Control group). After 1, 2, 3 or 4 months, the levels of Hb-AGEs and procollagen Ⅲ, collagen Ⅳ, collagen Ⅳ-AGEs and laminin were determined. Results Hemoglobin-AGEs (Hb-AGEs) in DM group was elevated significantly as compared with AG group and Control group; it increased with the prolongation of the time course of diabetes (after 1, 2, 3, and 4 months the Hb-AGEs was 6.88±1.23, 10.26±0.63, 15.3±1.49 and 18.57±2.90 ku/g, respectively), and was closely related to FBG. Procollagen Ⅲ of group DM increased monthly (after 1, 2, 3 and 4 months, it was 15.20±3.03, 21.44±1.79, 27.19±3.28, 33.99±4.96 μg/L, respectively) which was related to Hb-AGEs and collagen Ⅳ-AGEs, and was significantly higher than that of group AG and C ontrol group. Collagen Ⅳ acted in the same way as procollagen Ⅲ (it was 23.67±1.49, 30.37±2.86, 36.65±1.98 and 45.46±5.77 μg/L, respectively) with the correlation to Hb-AGEs and collagen Ⅳ-AGEs, so did the changes of collagen Ⅳ-AGEs (0.79±0.15, 1.25±O.22, 1.54±0.06 and 1.80±0.14 AGEs Mu/g in 1～4 months) with the correlation to Hb-AGEs and collagen Ⅳ. There was no difference of laminin among three groups. Conclusion It could be concluded that AGEs may be the cause of the increase of procollagen Ⅲ, collagen Ⅳ and collagen Ⅳ -AGEs in the aorta of diabetic rats, thus suggesting a role of AGEs in the development of atherosclerosis in diabetes mellitus.