晚期糖基化终末产物通过LOX-1调节HUVEC-12细胞CD40的表达  

Advanced Glycation Endproducts Regulate CD40 Expression in the Human Umbilical Vein Endothelial Cell via LOX-1

作　　者：尹凯[1] 桂庆军[1] 王北冰[1] 沈元琼[1] 游咏[1] 李熠[1] 涂玉林[2] 

机构地区：[1]南华大学诊断学教研室,湖南衡阳421001 [2]南华大学心血管病研究所

出　　处：《南华大学学报（医学版）》2010年第1期38-41,共4页Journal of Nanhua University(Medical Edition)

基　　金：湖南省科技厅项目(2007SK3092);湖南省卫生厅项目(B2007092)

摘　　要：目的研究晚期糖基化终末产物(AGEs)对人脐静脉内皮细胞株(HUVEC-12)细胞CD40表达的影响及凝集素样氧化低密度脂蛋白受体(LOX-1)的作用。方法实验分组:不同浓度(0,100、200、400、800 mg/L)的AGEs处理细胞24 h;400 mg/L的AGEs处理细胞不同时间(0、6、12、24 h);250μg/mL的LOX-1抑制剂PIA预处理后,加入200 mg/L的AGEs处理细胞。采用实时定量PCR和Western-blot技术分别检测各处理组HU-VEC-12细胞CD40 mRNA和蛋白质的表达。结果不同浓度AGEs处理细胞24 h,随着处理浓度增大,HUVEC-12细胞CD40的表达逐渐上调;400 mg/L的AGEs处理细胞不同时间,随着处理时间的延长,CD40表达逐渐增高;250μg/mL的PIA预处理细胞,明显下调AGEs诱导的HUVEC-12细胞CD40高表达,对正常状态下的CD40表达没有影响。结论AGEs诱导HUVEC-12细胞CD40表达上调,并存在量效和时效关系;LOX-1参与介导了AGEs作用下HUVEC-12细胞CD40的高表达。Objective To investigate the influence of Advanced Glycation Endproducts（AGEs）on CD40 expression in the human umbilical vein endothelial cell and the effect of Lectin-like oxLDL receptor-1（LOX-1） in this process. Methods HUVEC-12 cells were cultured and incubated with AGEs at different concentrations（0,100、200、400、800 mg/L）for the same time and at the same concentration for different time course（0、6、12、24 h）.Pretreated with LOX-1 blocking agent PIA（250 μg/mL）,HUVEC-12 cells were cultured with AGEs at 400mg/L for 24 h.The mRNA and protein expression of CD40 in different groups were detected by RT-PCR and Western blotting respectively. Results The expression of CD40 was significantly increased induced by AGEs in a dose-dependent manner within 0-800mg/l for 24h and in a time-dependent manner within 0-24h.Pretreatment with PIA（250μg/mL）attenuated the increased expression of CD40 induced by AGEs but had no effect on the basal expression of CD40. Conclusions AGEs up-regulated the expression of CD40 in a dose-dependent and time-dependent manner.This effect may be related to the mediation effect of LOX-1.

关 键 词：晚期糖基化终末产物 CD40 动脉粥样硬化 LOX-1 

分 类 号：R540.4[医药卫生—心血管疾病]