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。
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.
出处
《中华全科医学》
2009年第2期113-114,共2页
Chinese Journal of General Practice
基金
国家自然科学基金资助项目(30660058)