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目的:探讨糖基化终产物(AGEs))对人单核细胞源树突状细胞(DCs)血管细胞黏附分子-1(VCAM-1)表达的影响。方法:用免疫磁珠分离人外周血CD14+单核细胞,经含重组人粒细胞-巨噬细胞集落刺激因子(rhGM-CSF)100μg/L和重组人白细胞介素-4(rhIL-4)20μg/L的RPMI1640培养,使其分化为DCs,加入糖基化人血清白蛋白(AGE-HSA)200μg/ml,采用RT-PCR和Western blot法,观察AGE-HSA对DCs VCAM-1 mRNA和蛋白表达的影响,同时检测培养液上清中IL-12和IL-18的浓度。结果:与空白对照相比,AGE-HSA可上调DCs VCAM-1 mRNA和蛋白的表达(P<0.05),并且明显促进了DCs IL-12和IL-18的分泌(P<0.05)。AGE-HSA干预组与空白对照组相比差异无统计学意义(P>0.05)。结论:AGEs能够上调DCs VCAM-1的表达,并且促进DCs IL-12和IL-18的分泌,这可能是糖尿病通过DCs促进动脉粥样硬化发生的重要机制之一。
AIM: To investigate the effect of advanced glycation end products (AGEs) on the expression of vascular cell adhesion molecule-1 (VCAM-1) in human monocyte-derived dendritic cells (DCs). Methods: Human peripheral blood mononuclear cells (CD14 +) were isolated by immunomagnetic beads and cultured in the presence of 100 μg / L recombinant human granulocyte-macrophage colony stimulating factor (rhGM-CSF) and 20 μg rhG-4 / L of RPMI1640 culture, differentiate into DCs, adding glycosylated human serum albumin (AGE-HSA) 200μg / ml, using RT-PCR and Western blot method to observe the AGE-HSA DCs VCAM-1 mRNA and protein The effect of IL-12 and IL-18 in culture supernatants was also examined. Results: AGE-HSA upregulated the expression of VCAM-1 mRNA and protein (P <0.05) and promoted the secretion of IL-12 and IL-18 in DCs significantly compared with the blank control group (P <0.05). There was no significant difference between AGE-HSA intervention group and blank control group (P> 0.05). CONCLUSION: AGEs can up-regulate the expression of VCAM-1 in DCs and promote the secretion of IL-12 and IL-18 in DCs, which may be one of the important mechanisms for diabetes to promote atherosclerosis through DCs.