人巨细胞病毒感染致血管内皮细胞损伤机制的研究  

Mechanisms of vascular endothelial cell injury induced by human cytomegalovirus

作　　者：王凤[1] 吴建敏[1] 周亚滨[1] 李树英[1] 程轶喆[1] 齐眉[1] 唐伟[1] 王红[1] 刘娟[1] 于晗[1] 

机构地区：[1]实验畸形学教育部重点实验室山东大学医学院微生物学教研室,济南250012

出　　处：《山东大学学报（医学版）》2007年第11期1081-1084,共4页Journal of Shandong University:Health Sciences

基　　金：山东大学跨学科研究课题(2130053182042);山东省卫生厅课题(413940)

摘　　要：目的观察人巨细胞病毒(HCMV)感染对人血管内皮细胞氧化应激的影响及对血管细胞粘附分子-1(VCAM-1)和糖基化终产物受体(RAGE)时序性表达的影响,研究HCMV感染致动脉粥样硬化(AS)的作用机制。方法用HCMV感染血管内皮细胞,用激光共聚焦显微镜检测细胞内活性氧(ROS)的改变;采用RT-PCR方法检测不同感染时段细胞VCAM-1及RAGEmRNA的表达。结果HCMV感染血管内皮细胞后,HCMV组荧光强度显著高于对照组(P<0.01)。感染0 h时,VCAM-1 mRNA有基础水平的表达,4 h开始升高,8 h时达高峰,12 h开始回落,24 h回落更明显,与0 h比较,均有统计学意义(P<0.01),48 h接近0 h表达水平(P>0.05)。感染0 h时,RAGEmRNA有基础水平的表达,4 h开始升高,8 h时表达水平明显升高,随感染时间延长,表达量逐渐增高,感染24 h时达高峰,48 h开始回落,仍维持在较高的水平,各时段与0 h比较,均有统计学意义(P<0.01)。结论HCMV感染血管内皮细胞后能够增强氧化应激,促进VCAM-1及RAGE的mRNA表达,并且呈时间依赖性。HCMV有可能通过增强氧化应激、上调VCAM-1及RAGE的表达介导血管内皮细胞的炎症反应,促进动脉粥样硬化的发生、发展。Objective To explore the mechanisms of cytomegalovirus infection by investigating the changes of reactive oxygen species （ROS） and sequential changes of the vascular cell adhesion molecule-1 （VCAM-1） and the receptors for advanced glycation end products （RAGE） in vascular endothelial cells with human cytomegalovirus（HCMV） infec- tion. Methods Vascular endothelial cells were cultured and then infected by HCMV, then changes of reactive oxygen species were identified by confocal microscopy. Expressions of VCAM-1 and RAGE mRNA were determined by reverse transcriptase polymerase chain reaction. Results Fluorescence intensity was determined at a low level in the control group and was significantly increased in the HCMV group （P 〈 0.01）. VCAM-1 mRNA was expressed at a low level at 0 hour, began to increase at 4 hours after HCMV infection and reached a peak at 8 hours. After 12 hours, it began to decrease and significantly decreased at 24 hours, but it was higher than that at 0 hour （ P 〈 0.01 ）. At 48 hours, the VCAM-1 mRNA level was close to that at 0 hour （ P 〉 0.05）. RAGE mRNA was expressed at a low level in the control group, began to increase 4 hours after HCMV infection, increased to a significant level at 12 hours, and reached a peak at 24 hours. It significandy decreased but remained at a relatively high level at 48 hours （ P 〈 0.01 ）. Conclusions HCMV infection can enhance the oxidative stress and the expressions of VCAM-1 and RAGE mRNA in vascular endo- thelial cells and it may induce an inflammatory reaction by enhancing the oxidative stress and up-regulating the VCAM-1 and RAGE expressions in endothelial cells, which further facilitates the occurrence and development of atherosclerosis.

关 键 词：巨细胞病毒 脐静脉 活性氧 血管细胞粘附分子-1 糖基化终产物 受体 

分 类 号：R373[医药卫生—病原生物学]