HCMV感染致培养脐静脉内皮细胞活化和氧化应激的作用  

Role of HCMV infection in the activation and oxidative stress of cultured human umbilical vein endothelial cells

作　　者：脱厚珍[1] 车晶晶[1] 刘磊[2] 王佳伟[2] 冯子敬[1] 陈珺[1] 李继梅[1] 张拥波[1] 王得新[1] Tuo Houzhen Che Jingjing Liu Lei Wang Jiawei Feng Zijing Chen Jun Li Jimei Zhang Yongbo Wang Dexin(Department of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China. （ Tuo HZ, Che JJ, Feng ZJ, Chen J, Li JM, Zhang YB, Wang DX Department of Neurology, Tongren Hospital, Capital Medical University, Beijing 100730, China. （ Liu L, Wang JW)

机构地区：[1]首都医科大学附属北京友谊医院神经内科,北京100150 [2]首都医科大学附属同仁医院神经内科,北京100730

出　　处：《中华实验和临床病毒学杂志》2017年第4期298-301,共4页Chinese Journal of Experimental and Clinical Virology

摘　　要：目的 初步探讨人巨细胞病毒（HCMV）感染致内皮细胞损伤的机制.方法 体外培养人脐静脉内皮细胞（HUVEC）,以HCMV AD169株感染HUVEC,24 h后通过实时定量PCR方法检测细胞粘附分子VCAM-1 mRNA的表达.通过硝酸还原酶法检测细胞培养基中一氧化氮（N0）含量的变化.结果 HUVEC感染HCMV后24 h,VCAM-1 mRNA的表达水平较对照组明显增加,两组间差异具有统计学意义（P〈0.05）.感染HCMV后0-36 h的不同时间点,感染组细胞培养上清中NO含量均较对照组增加,呈现时间依赖性,各时间点两组间差异均具有统计学意义（P〈0.01）.结论 HCMV感染可增强内皮细胞氧化应激活动,可能在血管内皮细胞活化损伤过程中起重要作用..Objective To investigate the role of the activation and oxidative stress of cultured human umbilical vein endothelial cells （HUVEC） after HCMV infection.Methods HUVECs were divided into four groups：control,HCMV（＋）,after HCMV AD169 infection,and the supernatant of the culture was extracted,and the cells were lysed.The levels of vascular cellular adhesion molecule-1 （VCAM-1） in HUVEC were measured by real-time PCR.And the content of nitrogen nonoxide （NO） of the supernatant was detected by nitrate reductasemethod accordingly.Results Twenty-four hours after infection,the mRNA expression of VCAM-1 in HUVECs of HCMV infected group increased obviously compared to control,and NO quantity increased accordingly and time-dependently.There was significant difference between groups（P〈0.01）.Conclusions HCMV increases the mRNA expression of VCAM-1 and quantity of NO,which may contribute to the formation of AS.

关 键 词：动脉粥样硬化 巨细胞病毒 脐静脉内皮细胞 血管内皮粘附分子-1 氧化应激 

分 类 号：R373[医药卫生—病原生物学]