趋化因子FKN对外周血单个核细胞NF-κB和TNF-α表达的影响及卡托普利的干预作用  

Effect of chemotatic factor FKN on NF-κB and TNF-α expression in peripheral blood monocytes and intervention of Captopril

作　　者：孙健[1] 赵吉光[1] 郑柳颖[1] 雷明明[1] 郭惠娇[1] 杨春艳[1] 吴哲[1] 

机构地区：[1]吉林大学第二医院心血管内科,吉林长春130041

出　　处：《大连医科大学学报》2007年第5期438-441,共4页Journal of Dalian Medical University

摘　　要：[目的]通过研究趋化因子(fractalkine,FKN)对单个核细胞合成核因子-κB(nuclear factor?κappaB,NF-κB)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的影响,探索了FKN-CX3CR1可能存在的信号传导机制及在动脉粥样硬化形成中的作用,并探讨了卡托普利在这其中可能的干预作用。[方法]①抗凝血用Ficoll密度梯度离心法分离外周血单个核细胞。②将每份提取的单个核细胞分3组分别为:空白对照组、FKN组、卡托普利组。③应用免疫细胞化学法检测各组单个核细胞中NF-κB表达情况。④应用酶联免疫法检测各组培养液中TNF-α的表达水平。[结果]①FKN诱导组NF-κB(34.80±2.69)%和TNF-α(1506.1±69.3)pg/mL较空白组NF-κB(3.80±0.95)%和TNF-α(80.5±5.5)pg/mL表达显著增多(P<0.05)。②卡托普利干预组NF-κB(27.55±1.96)%和TNF-α(1119.3±116.2)pg/mL较FKN组NF-κB(34.80±2.69)%和TNF-α(1506.1±69.3)pg/mL表达显著减少(P<0.05)。[结论]FKN-CX3CR1有增加单个核细胞表达NF-κB、TNF-α的作用;而卡托普利可通过减弱FKN-CX3CR1诱导的单个核细胞合成NF-κB、TNF-α,抑制炎症反应。[ Objective] By researching the effects of Fractalkine（ FKN ） on the expression of NF - κB and TNF - α induced by FKN, We explore one of possible signal transduction pathways of FKN/CX3CR1 in atherosclerosis. And the invention of Captopril. [ Methods ] （1）Peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll - Paque gradient centrifugation. （2）Divide the extractive peripheral blood monocytes into three groups ：control, FKN and captopril groups. （3）Measure the NF - κB expression of monocytes from each group by immune cytochemsitry. （4）Collect the supernatant of monocytes from each group, determin the expression of TNF - α by enzyme - linked immunosorbent assay （ELISA）. [ Results ] （1）The expression of NF - κB （ 34.80 ± 2.69） % and TNF - α（ 1506.1 ± 69.3）pg/mL from FKN group was increased compared with the expression of NF - κB （3. 80 ± 0. 95 ）% and TNF - α（80.5 ±5.5）pg/mL from control group（P 〈0.05）. （2）The expression of NF - κB （27. 55 ± 1. 96）% and TNF - α（ 1119.3 ± 116.2 ） pg/mL from captopril group was decreased compared with the expression of NF - κB （ 34.80 ± 2.69 ） % and TNF - α （ 1506.1 ± 69.3 ） pg/mL from FKN group（ P 〈 0. 05 ）. [ Conclusions ] FKN - CX3CR1 increase the expressions of NF - κB and TNF - α in peripheral blood monocytes, which may be one of the mechanisms of contributing to the progression of atherosclerosis;Captopril participates in inhibiting inflammatory and preventing arteriosclerosis perhaps by reducing the expressions of NF - κB and TNF - α in peripheral blood monocytes induced by FKN -CX3CR1.

关 键 词：FKN 核因子-ΚB 肿瘤坏死因子 卡托普利 

分 类 号：R543.5[医药卫生—心血管疾病]