Objective-Both advanced glycosylation end products (AGEs) and dendritic cells (DCs) have been shown to play a causative role in atherosclerosis. However, whether they function interactively in the process remains uncertain. We therefore studied the effects of AGE-bovine serum albumin (AGE-BSA) on the maturation of DCs and the expressions of scavenger receptor-A (SR-A) and receptor for AGEs (RAGE) on DCs. Key Words: advanced glycosylation end products Ⅲ atherosclerosis Ⅲ dendritic cells Ⅲ immunity Ⅲ receptor for advanced glycosylation end products D iabetes is associated with severe atherosclerosis and cardiovascular diseases that account for a high mobility and mortality in industrialized countries. 1 It is therefore very important for us to understand the mechanisms of how the diseases occur. Advanced glycosylation end products (AGEs) (long-term products of the Maillard reaction) have been shown to play a causative role in diabetic vasculopathy and atherosclerosis. 2,3 In diabetic atherosclerotic lesions, not only the deposition of AGEs but also the colocalization of AGEs antigen and AGEs receptors (scavenger receptor A [SR-A], receptor for AGEs [RAGE]) were found. 2,3 Additionally, accumulating evidences have suggested that dendritic cells (DCs) also play a crucial role in atherosclerosis 4 by activating T-cell in atherosclerosis. 5 Proinflammatory factors can promote maturation of DCs corresponding to a switch from a phagocytic stage to a stage of strong T cell-stimulatory capacity. The interactive roles of AGEs and DCs remain unknown now. We therefore examined the effect of advanced glycosylation end-bovine serum albumin (AGE-BSA) on DCs maturation, cytokine secretion, and SR-A and RAGE expression. MethodsThe informed consent was obtained from all volunteers and the study protocol was approved by our institutional ethical committee.

Our study suggested that one of the anti-inflammatory mechanisms of PPAR-gamma agonist ciglitazone was mediated by inhibiting the ox-LDL induced maturation and immune function of DCs.

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