Objective It has been reported that advanced glycation end products (AGEs) participate in pathogenesis of accelerated atherosclerosis in diabetes through damaging endothelial function. Matrix metalloproteinases (MMPs) can be synthesized by endothelial cell and contribute to maintain endothelial homeostasis. The present work are aimed at Objective It has been reported that advanced glycation end products (AGEs) participate in pathogenesis of accelerated atherosclerosis in diabetes through damaging endothelial function. Matrix metalloproteinases (MMPs) can be synthesized by endothelial cells and contribute to maintain endothelial homeostasis. The present work are aimed at