摘要
目的探讨不规则趋化因子(FKN)在动脉粥样硬化形成中的作用及其可能的信号转导途径,以及FKN影响人单个核细胞表达NFκB过程与Ras/p38丝裂原活化蛋白激酶信号传导通路的相关性。方法采用密度梯度离心法分离人外周血单个核细胞,将细胞预处理后分为:空白1组、FKN 1组、FKN+Ras抑制剂组(FTI-277组)、空白2组、FKN 2组、FKN|p38抑制剂组(SB203580组)。分别于30 min时,采用Western blot方法对磷酸化p38及NF-κB进行半定量测定。结果与空白1组、空白2组比较,FKN 1组、FKN 2组NF-κB和p38相对吸光度值明显增加(P<0.01),与FKN 1组、FKN 2组比较,FTI-277组、SB203580组NF-κB和p38相对吸光度值明显降低(P<0.01)。结论 FKN可以使NF-κB表达和磷酸化p38增加;Ras/p38介导了FKN刺激单个核细胞引起NF-κB活化的增加;Ras/p38途径为FKN诱导NF-κB活化的信号转导通路之一。
Objective To investigate the role of fractalkine（FKN） in atherogenesis, to investigate the effect of FKN on the process of the expression of NF-κB in mononuclear cells,and its relation with the Ras/p38 MAPK signal transduction circuit. Methods Human peripheral blood mononu clear cells were isolated from fresh blood of healthy volunteers by Ficoll Paque gradient centrifu gation. The cells were divided into the following groups： control group one,FKN group one,Ras inhibitor group（FTI-277 group）, control group two, FKN group two and p38 inhibitor group （SB203580 group）. The phospho-p38 and NF-κB were measured semi-quantitatively by Western blot after 30 min. Results The relative integral absorbance of p38 and NF-κB from FKN groups one and two was significantly increased compared with the control groups one and two （P〈 0.01） ;the relative integral absorbance of NF -κB and p38 from FTI-277 group and SB203580 group was significantly lower compared with the FKN groups one and two （P 〈 0.01）. Conclusions FKN can increase the expression of NF-κB and phosphor-p38 in mononuclear cells. Ras and p38 mediate stimulating increase in activation of NF-κB in mononuclear cells by FKN. The Ras/ p38 pathway is one of signal transduetion pathways by which FKN induces activation of NF-κB.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2011年第7期646-648,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
吉林省科技发展计划项目(200705235)
