摘要
目的探索FKN-CX3CR1在单个核细胞中可能存在的信号传导途径及促进动脉粥样硬化形成的机制,并探讨蛋白激酶C(PKC)在其中的作用。方法(1)用Ficoll密度梯度离心法分离抗凝人外周血单个核细胞。(2)将每份提取的单个核细胞分为4组:对照组、FKN组、Ro31-8220(PKC特异性阻断剂)和PD98059(ERK1/2特异性阻断剂)组。(3)用Western blot法检测单个核细胞中磷酸化ERK1/2表达。(4)用ELISA法检测培养液中TNF-α的表达。结果(1)FKN组磷酸化的ERK1/2和TNF-α表达较对照组显著增多(P<0.05)。(2)Ro31-8220组磷酸化的ERK1/2和TNF-α表达较FKN组显著减少(P<0.05)。结论FKN-CX3CR1可能通过PKC/ERK途径诱导单个核细胞TNF-α的表达,最终促进动脉粥样硬化的形成和进展。
Objective To explore one of the potential signal transduction pathway of FKN/CX3CR1 in human peripheral blood monocytes （PBMC） and the mechanism of FKN in promoting atherosclerosis and to identify the function of protein kinase C. Methods （1）Human peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll-Paque gradient centrifugation. （2） Divided PBMC into four groups ： control, FKN, Ro318220 and PD98059 groups. （3） Measured the ERK 1/2 expression of monoeytes from each group by Western blot. （4） Collected the supernatant of monoeytes from each group, determined the expression of TNF-α by enzyme-linked immunosorbent assay（ELISA）. Results （1）The expression of ERK1/2 and TNF-α from FKN group was signifi- cantly higher as compared with the control. TNF-α from FKN group was significantly higher as compared with the control group（ P 〈 0.05 ）. （2）The expression of ERK1/2 and TNF-α from Ro31-8220 group was decreased as compared with FKN group （ P 〈 0. 05 ）. Conclusion FKN-CX3CR1 induces the expression of TNF-α via PKC/ERK signal pathway which may facilitate the development and progression of atherosclerosis.
出处
《基础医学与临床》
CSCD
北大核心
2009年第2期148-151,共4页
Basic and Clinical Medicine
基金
吉林省科技发展计划项目(200705235)
关键词
FKN
肿瘤坏死因子
蛋白激酶C
fractalkine
tumor necrosis factor
protein kinase C
