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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 irregular chemokines (FKN) in the development of atherosclerosis and its possible signal transduction pathways, as well as the effect of FKN on the expression of NFκB in human mononuclear cells and the activation of Ras / p38 mitogen-activated protein kinase Accessibility. Methods Human peripheral blood mononuclear cells were isolated by density gradient centrifugation. The cells were pretreated and divided into blank group 1, FKN 1 group, FKN + Ras inhibitor group (FTI-277 group), blank group 2 and FKN 2 group , FKN | p38 inhibitor group (SB203580 group). At 30 min, the phosphorylated p38 and NF-κB were semi-quantitatively determined by Western blot. Results Compared with blank group 1 and blank group 2, the relative absorbance values of NF-κB and p38 were significantly increased in FKN 1 group and FKN 2 group (P <0.01). Compared with FKN 1 group and FKN 2 group, FTI-277 group and SB203580 The relative absorbance of NF-κB and p38 were significantly decreased (P <0.01). Conclusion FKN can increase the expression of NF-κB and phosphorylation of p38. Ras / p38 mediate the activation of NF-κB induced by FKN in mononuclear cells. Ras / p38 pathway is the signal transduction pathway of NF-κB activation induced by FKN one.