糖基化终末产物诱导内皮微颗粒释放

Advanced glycation end products induce release of endothelial microparticle

目的观察糖基化终末产物(AGEs)对内皮微颗粒(EMP)释放的影响。方法予不同浓度AGEs(100、200、400μg/ml)干预人脐带静脉内皮细胞(HUVECs)12、24 h;分别予抗糖基化终末产物受体(RAGE)抗体、活性氧(ROS)清除剂预处理内皮细胞,再予400μg/ml AGEs干预内皮细胞24 h。检测以上各组EMP、RAGE、ROS。结果AGEs以浓度依赖方式,而非时间依赖方式诱导内皮细胞分泌EMP;同时,AGEs诱导内皮细胞RAGE、ROS表达水平增高。运用抗体阻断RAGE或ROS清除剂后,AGEs诱导产生的EMP水平下降。结论AGEs与RAGE相互作用,通过氧化应激途径诱导内皮微颗粒释放。

Objective To investigate whether advanced glycation end products(AGEs)have an effect on the release of endothelial microparticle(EMP).Methods Cultured human umbilical vein endothelial cells(HUVECs)were incubated with AGEs(100,200,400μg/ml)for 12 or 24 h.Pretreatment with anti-RAGE antibody or reactive oxygen species(ROS)scavenger,HUVECs were incubated with 400μg/ml AGEs for 24 h.EMP,RAGE and ROS were assessed.Results AGEs induced EMP releasing in a dose-dependent manner,not a time-dependent manner.Meanwhile,AGEs increased the levels of RAGE and ROS.Pretreatment with anti-RAGE antibody or antioxidant treatment could reverse the release of AGEs inducing EMP.Conclusion AGEs-RAGE interaction induced EMP generation,which was mediated by oxidative stress.