内皮功能障碍
伊诺斯
内分泌学
内科学
糖尿病
过氧亚硝酸盐
NADPH氧化酶
医学
氧化应激
链脲佐菌素
内皮
发病机制
一氧化氮
超氧化物
化学
一氧化氮合酶
生物化学
酶
作者
Wei Zhang,Fang Fu,Ru Tie,Xue Liang,Fei Tian,Wenjuan Xing,Jingya Li,Lele Ji,Jinliang Xing,Xin Sun,Haifeng Zhang
出处
期刊:VASA
[Hogrefe Publishing Group]
日期:2013-11-01
卷期号:42 (6): 421-428
被引量:32
标识
DOI:10.1024/0301-1526/a000311
摘要
Background: Endothelial dysfunction is an important factor in the pathogenesis of diabetes related vascular complications, and acute alpha-linolenic acid (ALA) intake can increase flow-mediated dilation of the diabetic artery at 4 h postprandially. However, whether chronic ALA supplementation may prevent endothelial dysfunction in the process of diabetes and underlying mechanisms remains largely unknown. Materials and methods: The high-fat diet-fed streptozotocin (HFD-STZ) rats provided an animal model for T2DM. Age-matched normal and HFD-STZ rats randomly received normal diet or ALA (500 mg/kg per day). After 5 weeks of feeding, endothelial function was determined. Results: Diabetes caused significant endothelial dysfunction (maximal vasorelaxation responses to ACh) in aortic segments, and ALA intake alleviated endothelial dysfunction. Superoxide production and peroxynitrite (ONOO-) formation were reduced with ALA supplement in diabetic vascular segments. Interestingly, ALA intake enhanced eNOS but inhibited iNOS activity in diabetic vessels. Moreover, ALA intake significantly increased eNOS phosphorylation. On the other hand, gp91phox and iNOS overexpression were reduced moderately with ALA intake in diabetic vessels. Conclusions: We concluded that ALA prevents diabetes-induced endothelial dysfunction by enhancing eNOS activity and attenuates oxidative/nitrative stress by inhibiting iNOS and NADPH oxidase expression and ONOO- production.
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