摘要
目的通过研究FKN对单个核细胞合成NF-κB、TNF-α的影响,探索了FKN-CX3CR1可能存在的一条信号传导机制,并探讨了核因子-κB在其中的作用。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、PDTC组。(3)应用免疫组化检测各组单个核细胞中NF-KB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(1)FKN诱导组较空白组NF-κB、TNF-α表达明显增多。(2)NF-κB阻断剂PDTC组较FKN组TNF-α表达明显减少。结论(1)FKN-CX3CR1有促进动脉粥样硬化形成的作用,其机制之一可能是通过增加单个核细胞表达NF-κB、TNF-α而实现的。(2)FKN可能通过激活NF-κB,进而促进TNF-α的表达。
Objective By researching the effects of FKN to the expression of NF-κB and TNF-α induced by FKN, We explore one of possible signal conductive mechanisms of FKN/CX3CR1 and the function of Nuclear factor -κppaB. 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 six groups： control group, FKN group, PKC inhibitor RO31-8220 group. （3） measure the Nuclear factor κppaB expression of monocytes from each group by immune histochemsitry. （4）Collect the supematant of monocytes from each group, determin the expression of TNF-α by enzyme-linked immunosorbent assay（ELISA）. Results （1）The expression of NF-κB and TNF-α from FKN group is increased compared with the control group . （2）The expression of TNF-α from inhibitor NF-Kb PDTC group is decreased compared with the FKN group. Conclusion （1）FKN-CX3CR1 increase the expressions of NF-κB and TNF- αin Peripheral blood monocytes as one of the mechanisms of contributing to the progression of atherosclerosis. （2）By activating NF-κB FKN improves the expression of TNF-α
出处
《中国实验诊断学》
2008年第6期721-724,共4页
Chinese Journal of Laboratory Diagnosis
基金
吉林省科技发展计划项目资助(项目编号:200705235)
