中文摘要：

目的探讨2型糖尿病大鼠胸主动脉内皮依赖血管舒张功能的改变及其机制。方法高脂高糖饮食加小剂量链脲佐菌素建立2型糖尿病大鼠模型，分组处理4周后，观察糖尿病（DM）组、正常（NC）组、糖基化终末产物抑制剂（AG）组血管舒张功能，eNOSmRNA表达及血清NO浓度。结果①DM组血糖、血清胰岛素、甘油三酯较NC组显著升高（P〈0．05）。②最大内皮依赖血管舒张功能（EDVRmax），DM组低于AG组（P〈0．05），AG组低于NC组（P〈0．05）。③eNOSmRNA表达，AG组高于DM组（P〈0．05），DM组高于NC组（P〈0．05）。④血清NO浓度AG组高于NC组（P〈0．05），NC组高于DM组（P〈0．05）。结论高级糖基化终末产物（AGEs）通过NO途径介导糖尿病内皮功能损伤，糖基化终末产物抑制剂（AG）可改善内皮依赖血管舒张功能。

英文摘要：

Objective To study the change of aortic endothelium-dependent vasodilation function in type 2 diabetic rats and its mechanism. Methods Male SD rats were injected with low dose Streptozotocin and fed with diets enriched in fat and sugar to form type 2 diabetic model. Then, the rats were managed in 3 groups, normal group （ NC）, diabetes group （ DM ）, diabetes with Aminoguanidine（AG） group. After 4 weeks, the Ach-dependent vasodilation response of isolated aorta, the expression of eNOS mRNA in the aorta, the synthesis of nitric oxide（NO） in serum were detected. Results ① Fast plasma glucose（ FPG）, insulin （ FINS）, triglyceride （TG） levers in DM groups were significantly higher than that in NC groups （ P 〈 0. 05 ）. ② The maximum acetylcholine（Ach）-dependent vasodilation response （EDVRmax） of aorta decreased significantly in DM, AG groups compared with that in NC groups （ P 〈 0. 05 ） ; EDVRmax in DM groups significantly reduced than that in AG groups （P 〈 0. 05 ）. ③The eNOS mRNA expression in DM groups were significantly higher than that in NC groups （ P 〈 0. 05 ）, but lower than that in AG groups （ P 〈 0. 05 ）. ④ NO concentration were significantly higher in AG groups （ P 〈 0. 05 ） ; but those in DM groups were significantly lower than that in NC groups （P 〈 0. 05）. Conclusion Advanced glycation end products （AGEs） damaged the function of vascular endothelium though nitric oxide pathway and inhibitor Aminoguanidine（AG） can get an improved EDVR.