【摘 要】
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Objective Advanced glycation end products(AGEs) and vascular adveentitial fibroblasts(AFs) are involved in diabetes-related vascular complications.However,the effect of AGEs on AFs remains unclear.The
【机 构】
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Department of Cardiology,Second Hospital Affiliated to the Second Military Medical University,Shangh
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Objective Advanced glycation end products(AGEs) and vascular adveentitial fibroblasts(AFs) are involved in diabetes-related vascular complications.However,the effect of AGEs on AFs remains unclear.The aim of this study was to observe the impact of AGEs on cell migration capacity and associated inflammatory responses of AFs.Methods Isolated vascular AFs of Sprague-Dawley rats were cultured,harvested after 24 h synchronization and challenged with AGE-HSA.Results AGE-HSA upregulated the expression of receptor for advanced glycation end products(RAGE),significantly increased the migration capacity and inflammatory mediators MCP-1,IL-6,VCAM-1 expressions on AFs.These effects could be significantly attenuated by anti-RAGE neutralizing antibody,p38,ERK1/2 and JNK MAPK inhibitors as well as by candesartan.AGE-HAS also upregnlated NF-κB transcriptional activity and I-κB-α phosphorylation,effect that was significantly inhibited by candesartan.Conclusion AGE-HSA increased the migration capacity and inflammatory responses of rat AFs via RAGE-MAPK-NF-κB pathways.Candesartan effectively inhibited these effects which might be a novel vascular protection mechanism of candesartan.
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