流感病毒感染与血管内皮细胞功能变化的体外实验研究  

The Study of Relationship between Influenza Virus Infection and the Dysfunction of Vascular Endothelial Cells in Vitro

作　　者：关秀茹[1] 王优良[1] 张萱[1] 林春艳[1] 韩丽[1] 杜柏岩[1] 

机构地区：[1]哈尔滨医科大学附属第一医院,黑龙江省哈尔滨市150001

出　　处：《中国动脉硬化杂志》2011年第8期641-644,共4页Chinese Journal of Arteriosclerosis

基　　金：黑龙江省自然科学基金资助项目(D200968)

摘　　要：目的探讨流感病毒感染人脐静脉内皮细胞后,细胞间黏附分子1和血管细胞黏附分子1表达的变化,以期从细胞和分子水平探讨流感病毒感染在动脉粥样硬化形成中的作用。方法分别运用染料结合实时荧光定量聚合酶链反应方法、流式细胞术和酶联免疫吸附实验,检测流感病毒感染的不同时段(0、24、48、72 h)人脐静脉内皮细胞分泌的细胞间黏附分子1、血管细胞黏附分子1的表达情况。结果流感病毒感染人脐静脉内皮细胞后,通过以上3种方法检测细胞间黏附分子1和血管细胞黏附分子1的变化,0 h有基础水平的表达,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,72 h表达量仍维持在较高的水平,显著高于未加病毒的对照组,各时段与对照组比较,均有统计学意义(P<0.05)。结论流感病毒感染人脐静脉内皮细胞后,细胞间黏附分子1和血管细胞黏附分子1表达增加,因此推测流感病毒感染导致血管内皮细胞功能障碍,流感病毒感染可能参与动脉粥样硬化的炎症反应。Aim To explore the mechanisms of influenza virus infection in the formation of atherosclerosis from the cellular and molecular levels through investigating amount of intercellular adhesion molecule-1and vascular cell adhesion molecule-1after human umbilical vein endothelial cell was infected by influenza virus. Methods SYBR Green reverse transcription polymerase chain reaction（RT-PCR）,flow cytometry and enzyme-linked immunosorbent assay were used to detect the timing expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 of human umbilical vein endothelial cells infected by influenza virus at 0 h,24 h,48 h and 72 h. Results Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1were measured by these three methods after human umbilical vein endothelial cell was infected by influenza virus.The base level of the two inflammatory factors was expressed at a low level at 0 h,and began to increase after influenza virus infection,reached the peak at 24 h.After 48 h,it declined obviously and remained a relatively high level at 72 h.The amount of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the infected groups was higher than that in the control group（P﹤0.05）. Conclusion This study showed that influenza virus infection could increase the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1,and then influenza virus infection might lead to dysfunction of vascular endothelial cells and involve in the inflammatory response of atherosclerosis.

关 键 词：动脉粥样硬化 流感病毒 内皮细胞 细胞间黏附分子1 血管细胞黏附分子1 

分 类 号：R5[医药卫生—内科学]