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-kB、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-1 mRNA表达水平与外周血oxLDL水平、NF-kBp65、ICAM-1 mRNA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-kB,上调ICAM-1的表达,导致糖尿病早期内皮功能障碍.

abstractsDiabetic 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 lowdensity lipoprotein receptor-1 ( LOX-1 ),NF-kB,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-kB,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-kB and up-regulating ICAM-1 expression.