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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。
Objective To investigate the changes and mechanisms of endothelium-dependent vasodilation in the thoracic aorta of type 2 diabetic rats. Methods The model of type 2 diabetic rats was established by high-fat and high-sugar diet combined with low-dose streptozotocin. After 4 weeks of treatment, the effects of diabetes mellitus (DM), normal group (NC), advanced glycation endproduct inhibitor AG) group, vasodilation function, eNOS mRNA expression and serum NO concentration. Results ① The levels of blood glucose, serum insulin and triglyceride in DM group were significantly higher than those in NC group (P <0.05). ② The maximal endothelium-dependent vasodilatation (EDVRmax) was lower in DM group than in AG group (P <0.05), AG group was lower than NC group (P <0.05). ③eNOS mRNA expression in AG group was higher than that in DM group (P <0.05), DM group was higher than NC group (P <0.05). Serum NO concentration in AG group was higher than that in NC group (P <0.05), NC group was higher than DM group (P <0.05). CONCLUSION: Advanced glycation end products (AGEs) mediate the endothelial dysfunction through the NO pathway. The advanced glycation end products (AGs) can improve endothelial dependent vasodilatation.