内分泌学
内科学
GTP环水解酶I
内皮
主动脉
内皮功能障碍
体内
乙酰胆碱
一氧化氮
血管舒张
医学
四氢生物蝶呤
生物
一氧化氮合酶
生物技术
作者
Yan Ling,Jiqianzhu Zhang,Xiaoyu Dai,Jinfeng Liu,Fangyuan Gao,Xiaofang Zhang,Yijun Tian,Wenjing Shi,Jian Zhu,Ji-Kuai Chen
出处
期刊:Journal of Vascular Research
[S. Karger AG]
日期:2021-01-01
卷期号:58 (2): 134-138
被引量:2
摘要
This study tested the hypothesis that endothelium-specific GTP cyclohydrolase I (GTPCH I) overexpression (Tg-GCH) restores age-associated endothelial dysfunction in vivo. Aortic GTPCH I expression and serum nitric oxide (NO) release were measured in young and aged mice. Aortic rings from young and aged wild-type (WT) mice and aged Tg-GCH mice were suspended for isometric tension recording. A hind limb ischemia model was used to measure blood flow recovery. Aged mice showed reduced GTPCH I expression in the aorta and decreased NO levels in serum. Compared with aged WT mice, Tg-GCH significantly elevated NO levels in serum in aged Tg-GCH mice, restored the impaired aortic relaxation in response to acetylcholine, and significantly elevated aortic constriction in response to L-NAME. Importantly, aged Tg-GCH mice displayed a significant increase in blood flow recovery compared with aged WT mice. GTPCH I reduction contributes to aging-associated endothelial dysfunction, which can be retarded by Tg-GCH.
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