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

关键词:  FKN  核因子－κB  肿瘤坏死因子  卡托普利

Key words:  fractalkine  nuclear factor –κappaB  tumor necrosis factor –α  Captopril

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。

Abstract:

［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］①Peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll-Paque gradient centrifugation.②Divide the extractive peripheral blood monocytes into three groups :control,FKN and captopril groups.③Measure the NF-κB expression of monocytes from each group by immune cytochemsitry.④Collect the supernatant of monocytes from each group,determin the expression of TNF-α by enzyme-linked immunosorbent assay(ELISA).［Results］①The 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）.②The 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－αin peripheral blood monocytes induced by FKN-CX3CR1.