趋化因子FKN对外周血单核细胞NF-κB和TNF-α表达的影响及蛋白激酶C在其中的作用  

Effect of Fractalkine on NF-κB and TNF-α expression in peripheral blood monocytes and role of protein kinase C

作　　者：郑柳颖[1] 孙健[2] 雷明明[3] 郭惠娇[2] 侯文丽[2] 吴哲[2] 

机构地区：[1]天津市第五中心医院心内科,天津塘沽300450 [2]吉林大学第二临床医学院心内科,吉林长春130041 [3]中国医科大学附属第四医院心内科,辽宁沈阳110032

出　　处：《大连医科大学学报》2008年第4期310-313,共4页Journal of Dalian Medical University

基　　金：吉林省科技发展计划项目资助课题(200705235)

摘　　要：[目的]对单核细胞合成核因子-κB(nuclear factor-κappaB,NF-κB)、肿瘤坏死因子-α(tumor necrosisfactor-α,TNF-α)的影响,探讨趋化因子(fractalkine,FKN)-CX3CR1可能存在的信号转导机制及在动脉粥样硬化形成中的作用,并探讨了蛋白激酶C(protein kinase C,PKC)的介导作用。[方法]①Ficoll密度梯度离心法分离外周血单核细胞。②每份提取的单核细胞分为空白对照组、FKN、RO31-8220(PKC特异性阻断剂)组。③免疫细胞化学法检测各组单核细胞中NF-κB的表达。④酶联免疫法检测各组培养液中TNF-α的表达水平。[结果]FKN、RO31-8220与空白对照组的NF-κB的阳性细胞率分别为(34.80±2.69)%,(20.10±2.78)%与(3.80±0.95)%(三组间差异P<0.05);TNF-α含量分别为(1506.1±69.3)pg/mL,(820.2±22.8)pg/mL,(80.5±5.5)pg/mL(三组间差异P<0.05)。[结论]FKN-CX3CR1能增加NF-κB、TNF-α单核细胞的表达;而FKN与CX3CR1结合以后,可能通过激活细胞内蛋白激酶C,进而诱导单核细胞合成NF-κB、TNF-α。[Objective] The effect of Fractalkine（FKN）on the expression of NF-κB 、TNF-αand the role of protein kinase C were investigated.[Methods]①Peripheral blood monocytes were isolated by Ficoll-Paque gradient centrifugation.②The monocytes were divided into ： FKN、RO31-8220 and control groups.③The NF-κB expression of the monocytes in each group was detected by immune cytochemsitry.④The level of TNF-α in the supernatant of monocytes from each group was determined by enzyme-linked immunosorbent assay（ELISA）.[Result]In FKN,RO31-8220 and control groups,the expression rates of NF-κB were（34.80±2.69）%,（20.10±2.78）% and（3.80±0.95）% respectively（P〈0.05）;and levels of TNF-α were（1506.1±69.3）pg/mL,（820.0±22.8）pg/mL and（80.5±5.5）pg/mL respectively（P〈0.05）.[Conclusions]FKN-CX3CR1 may increase the expressions of NF-κB and TNF-α in peripheral blood monocytes and FKN initiates intracellular signal conductive mechanism with activating PKC.

关 键 词：FKN 核因子-ΚB 肿瘤坏死因子 蛋白激酶C 

分 类 号：R341[医药卫生—基础医学]