2型糖尿病大鼠血管内皮功能改变及机制

被引：6

作者：

李丽 ^{[1
,2
]}

黄起壬 ^{[3
]}

机构：

[1] 江西省南昌大学医学院

[2] 九江县人民医院内科

[3] 江西省南昌大学药学院

来源：

中华全科医学 | 2009年 / 7卷 / 02期

关键词：

高级糖基化终末产物(AGEs); 2型糖尿病; 内皮依赖血管舒张功能; 内皮型一氧化氮合酶(eNOS);

D O I：

10.16766/j.cnki.issn.1674-4152.2009.02.028

中图分类号：

R587.1 [糖尿病];

学科分类号：

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。

引用

页码：113 / 114

页数：2

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