0xLDL／LOX-1系统及NF—κB通路在糖尿病血管内皮功能障碍中的作用机制  

Role of oxLDL/LOX-1 system and NF-κB pathway in early diabetic vascular endothelial dysfunction

作　　者：张立功[1] 王立俊[2] 刘海燕[2] 于永慧[2] 汪翼[2] 

机构地区：[1]山东大学附属省立医院麻醉科,济南250021 [2]山东大学附属省立医院儿科,济南250021

出　　处：《中华内分泌代谢杂志》2012年第7期589-592,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：基金项目：山东省优秀中青年科学家科研奖励基金项目（BS2010YY056,2006BS03065）

摘　　要：腹腔注射链脲佐菌素建立糖尿病大鼠模型（DM组），结果显示糖尿病大鼠2周时氧化低密度脂蛋白（oxLDL）水平已高于正常对照大鼠[（2．87±0．40对2．27±0．36）μg／dl，P〈0．05]，血管舒张反应迟钝；6周时oxLDL水平更高[（4．32--0．66）μg/dl，P〈0．01]，乙酰胆碱诱导的血管环舒张最大百分比（Rmax）明显降低（P〈0．01），糖尿病大鼠主动脉植物血凝素样氧化低密度脂蛋白受体1（LOX-1）、NF—κB、内皮细胞间黏附分子1（ICAM-1）蛋白及mRNA表达明显高于正常对照大鼠（P〈0．01），糖尿病大鼠LOX-1mRNA表达水平与外周血oxLDL水平、NF-κBp65、ICAM-1mRNA表达水平正相关，与Rmax呈负相关。提示OxLDL／LOX-1系统可能通过激活NF-κB，上调ICAM-1的表达，导致糖尿病早期内皮功能障碍。[ Summary ] Diabetic rat model was established by peritoneal injection of streptozocin. At the end of 2 weeks, oxidized low-density lipoprotein （oxLDL） level in diabetic rats was raised [ （2.87 ±0.40 vs 2.27± 0.36 ） μg/dl, P〈 0.05 ] and endothelium-dependent relaxation was sluggish compared with normal rats. At the end of 6 weeks, oxLDL level continued to increase [ 4.32± 0.66 ） μg/dl, P〈0.01 ] and endothelium-dependent maximum relaxation （ Rmax ） was decreased obviously （P〈 0. 01 ）. Meanwhile, the protein and mRNA expressions of lectin-like oxidized low- density lipoprotein receptor-1 （ LOX-1 ） , NF-κB, and ICAM-1 on vessel wall of diabetic rats were higher than those in normal rats, and LOX-1 mRNA was positively correlated with the levels of oxLDL, NF-κB, and ICAM-1 mRNA, while negatively correlated with Rmax, indicating that OxLDL/LOX-1 system may cause early endothelial dysfunction in diabetes via activating NF-κB and up-regulating ICAM-1 expression.

关 键 词：糖尿病 氧化低密度脂蛋白 植物血凝素样氧化低密度脂蛋白受体1 NF-κB 血管内皮功能障碍 

分 类 号：R587.2[医药卫生—内分泌]