中文摘要：

目的探讨内脂素在高糖状态下对血管内皮细胞单核细胞趋化蛋白1（MCP-1）和细胞间黏附分子1（ICAM-1）蛋白表达的影响及机制。方法体外培养人脐静脉内皮细胞（HUVEC）分为3组：空白对照组（0mmol/L葡萄糖处理）、生理葡萄糖组（5.5mmol/L葡萄糖处理）、高糖组（25mmol/L葡萄糖处理）,分别用不同浓度内脂素（0、10、50、100ng/ml）培养24h。另取HUVEC,在p38MAPK特异性抑制剂SB203580预处理30min后,加入内脂素（100ng/ml）及葡萄糖（0、5.5、25mmol/L）培养24h。采用反转录-聚合酶链反应（RT-PCR）检测HUVEC中p38MAPKmRNA表达量,采用Westernblotting检测HUVEC中磷酸化p38MAPK蛋白表达水平,并用双抗体夹心酶联免疫吸附试验（ELISA）检测细胞培养上清液中的MCP-1、ICAM-1蛋白表达量。结果空白对照组、生理葡萄糖组中,内脂素促进HUVEC中p38MAPKmRNA转录、p38MAPK蛋白磷酸化以及MCP-1、ICAM-1蛋白的表达,并呈浓度依赖性（P〈0.01）;与空白对照组和生理葡萄糖组相比,高糖组内脂素进一步增强HUVEC中p38MAPKmRNA、磷酸化p38MAPK蛋白和MCP-1、ICAM-1蛋白的表达（P〈0.05）。SB203580预处理后,内脂素（100ng/ml）在3种不同浓度葡萄糖状态下对HUVEC内p38MAPK蛋白磷酸化以及MCP-1、ICAM-1蛋白表达量的影响均显著降低（P〈0.01）。结论内脂素可能通过激活p38MAPK信号通路促进HUVEC表达MCP-1和ICAM-1蛋白,并呈剂量依赖性。高浓度（25mmol/L）葡萄糖可增强内脂素促进HUVEC内MCP-1和ICAM-1蛋白表达的作用,进一步加速血管内皮细胞功能受损。

英文摘要：

Objective To investigate the effects of visfatin on the expression of monocyte chemoattractant protein-1 （MCP-1） and intercellular adhesion molecule-1 （ICAM-1） in vascular endothelial cells under high glucose condition and the underlying mechanism.Methods Human umbilical vein endothelial cells （HUVECs） were cultured in vitro and divided into 3 groups：control group （0mmol/L glucose）,normal glucose group （5.5mmol/L glucose） and high glucose group （25mmol/L glucose）.HUVECs were incubated with human recombinant visfatin in various concentrations （0,10,50 and 100ng/ml） for 24 hours.Other specimens of HUVECs were pretreated for 30 minutes with SB203580,a specific inhibitor of p38 mitogen-activated protein kinase （p38MAPK） signal pathway,and then incubated with 100ng/ml visfatin and glucose in various concentrations （0,5.5 and 25mmol/L） for 24 hours.The expressions of MCP-1 and ICAM-1 in HUVECs were examined with enzyme-linked immunosorbent assay （ELISA）,the expression of p38MAPK mRNA in HUVECs was determined with reverse transcription-polymerase chain reaction （RT-PCR）,and the proteins of phosphor-p38MAPK in HUVECs were analyzed by Western blotting.Results The transcription of p38MAPK mRNA,the phosphorylation of p38MAPK proteins,and the expressions of MCP-1 and ICAM-1 in HUVECs were significantly promoted by visfatin in a dose-dependent manner in control group and normal glucose group （P0.01）.Under high glucose condition （25mmol/L）,visfatin showed a synergetic effect on stimulating the expressions of p38MAPK mRNA,phosphor-p38MAPK proteins,and MCP-1 and ICAM-1 proteins （P0.05）.Pretreatment with SB203580 significantly inhibited the effects of visfatin in promoting the phosphorylation of p38MAPK and the expressions of MCP-1 and ICAM-1 proteins （P0.01）.Conclusion Visfatin,which has recently been indentified as a novel visceral adipokine,is a vascular proinflammatory cytokine,and it may promote the expressions of the inflammatory MCP-1 and ICAM-1 in a dose-depend