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目的探讨铁调素(hepcidin)对血管内皮细胞(vascular endothelial cell,VEC)炎症通路中核转录因子κB(Nuclear Factor-κB,NF-κB)家族的影响。方法使用不同浓度的人铁调素处理人脐静脉内皮细胞(human umbilical vein endothelial cell;HUVEC)24h后,利用蛋白印迹技术(Western blot)检测细胞中核转录因子κB抑制蛋白α(inhibitor of NF-κB;IκBα)、细胞间粘附分子(intercellular adhesion molecule-1,ICAM-1)的蛋白表达;免疫荧光法观察NF-κB p65转核、ICAM-1蛋白表达;体外粘附实验检测干预后的HUVEC的粘附能力。结果铁调素能剂量依赖的降低HUVEC中IκBα及促进ICAM-1表达,其中干预剂量大于300 ng/ml处理组时的相比对照组差异均具有统计学意义(P<0.05);激光共聚焦成像结果显示,600 ng/ml铁调素处理24h后,HUVEC中NF-κB p65转入核内,ICAM-1蛋白表达增加;粘附实验的结果显示,剂量量大于75 ng/ml铁调素处理能剂量依赖性的上调HUVEC的粘附能力,与对照组相比差异均具有统计学意义(P<0.05)结论铁调素可诱导血管内皮细胞IκBα的下调,促使NF-κB p65转核,升高血管内皮细胞ICAM-1的表达水平。铁调素可通过调控NF-κB通路介导血管内皮细胞炎症反应。[营养学报,2014,36(1):31-34]
Objective To investigate the effect of hepcidin on the nuclear factor-κB (NF-κB) family in inflammatory pathways of vascular endothelial cells (VECs). Methods Human umbilical vein endothelial cells (HUVECs) were treated with different concentrations of human hepcidin for 24 h. Western blotting was used to detect the expression of inhibitor of NF-κB ; IκBα), intercellular adhesion molecule-1 (ICAM-1) protein expression; immunofluorescence staining NF-κB p65 transfection, ICAM-1 protein expression; in vitro adhesion assay after intervention of HUVEC The adhesion capacity. Results Hepcidin dose-dependently reduced the expression of IκBα and ICAM-1 in HUVECs, and the difference was significant compared with the control group when the intervention dose was more than 300 ng / ml (P <0.05) The results of imaging showed that after NF-κB p65 was transfered to nucleus in HUVEC at 24h after 600 ng / ml hepcidin treatment, the expression of ICAM-1 protein increased. Adhesion experiments showed that the dose of heparin was higher than 75 ng / ml hepcidin (P <0.05) Conclusions Hepcidin can induce the down-regulation of IκBα in vascular endothelial cells and promote the nuclear translocation of NF-κB p65.Conclusion Hepcidin can up-regulate the adhesion of HUVECs in a dose-dependent manner, Increase the expression of ICAM-1 in vascular endothelial cells. Hepcidin can mediate the inflammatory reaction of vascular endothelial cells by regulating NF-|ÊB pathway. [Journal of Nutrition, 2014,36 (1): 31-34]