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目的探讨在动脉粥样斑块硬化进程中C反应蛋白(CRP)和酶修饰低密度脂蛋白(E-LDL)对外周血中树突状细胞(DC)分化成熟的影响。方法梯度离心法分离人外周血单核细胞,用含rhGM-CSF和rhIL-4的Cellgro培养液培养5d,使其分化为DC。分别用CRP、E-LDL及CRP加E-LDL刺激DC48h后,采用流式细胞术检测DC表型(CD1a、CD80、CD86、HLA-DR)的表达,ELISA法检测DC上清液中IL-12、TNFα、IL-2和IL-10的含量,并进行比较。结果CRP抑制DC的CD1a、CD80表达及IL-12、TNFα分泌,E-LDL促进DC的CD1a、CD80、CD86和HLA-DR表达及IL-12、TNFα分泌,CPR加E-LDL结果与E-LDL类似。结论CRP抑制DC的活化,E-LDL可促进DC的分化成熟,E-LDL激活DC的作用强于CRP的抑制作用。
Objective To investigate the effect of C-reactive protein (CRP) and enzyme-modified low-density lipoprotein (E-LDL) on the differentiation and maturation of peripheral blood dendritic cells (DCs) during atherosclerotic plaque progression. Methods Human peripheral blood mononuclear cells were isolated by gradient centrifugation and cultured in Cellgro medium containing rhGM-CSF and rhIL-4 for 5 days to differentiate into DC. The DC phenotypes (CD1a, CD80, CD86, HLA-DR) were detected by flow cytometry after stimulating DC48h with CRP, E-LDL, CRP and E-LDL respectively. 12, TNFα, IL-2 and IL-10 levels, and compared. Results CRP inhibited the expression of CD1a and CD80 and the secretion of IL-12 and TNFα. E-LDL promoted the expression of CD1a, CD80, CD86 and HLA-DR and the secretion of IL-12 and TNFα in DCs. LDL similar. Conclusion CRP can inhibit the activation of DC, E-LDL can promote the differentiation and maturation of DC, and the effect of E-LDL activation DC is stronger than that of CRP.