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| 内皮型一氧化氮合酶脱偶联的研究进展 | |
| 引用本文： | 郑建普,卞卡,可燕,MURAD Ferid. 内皮型一氧化氮合酶脱偶联的研究进展[J]. 中国药理学通报, 2006, 22(6): 659-663 |
| 作者姓名： | 郑建普 卞卡 可燕 MURAD Ferid |
| 作者单位： | 1. 上海中医药大学穆拉德中药现代化研究中心,上海,201203 2. 上海中医药大学穆拉德中药现代化研究中心,上海,201203;上海高校一氧化氮与炎症医学研究院,上海,201203;美国德克萨斯大学休斯顿医学院综合生物及药理学系,德克萨斯大学分子医学研究所,休斯顿,TX 77030 3. 上海中医药大学穆拉德中药现代化研究中心,上海,201203;上海高校一氧化氮与炎症医学研究院,上海,201203 4. 上海中医药大学穆拉德中药现代化研究中心,上海,201203;美国德克萨斯大学休斯顿医学院综合生物及药理学系,德克萨斯大学分子医学研究所,休斯顿,TX 77030 |
| 基金项目： | 上海市教委资助项目;上海市教委资助项目;上海市科委资助项目 |
| 摘 要： | 血管内皮功能障碍(endothelial dysfunction)是多种心脑血管疾病的共同病理机制,其突出表现为内皮依赖性血管舒张功能障碍,主要由NO减少及氧自由基增加所致。最新研究发现,内皮型一氧化氮合酶脱偶联(eNOS uncoup ling)是导致NO水平下降和氧自由基水平升高的重要机制,是高血压、糖尿病、动脉粥样硬化等疾病中内皮功能障碍的重要原因。通过纠正eNOS脱偶联可有效改善内皮功能,有望为保护血管内皮功能提供有效途径。 |
| 关 键 词： | eNOS脱偶联 内皮功能障碍 一氧化氮 氧化应激 四氢生物蝶呤 |
| 文章编号： | 1001-1978(2006)06-0659-05 |
| 收稿时间： | 2006-02-22 |
| 修稿时间： | 2006-04-16 |
Research progress on endothelial nitric oxide synthase uncoupling |
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| ZHENG Jian-pu,BIAN Ka,KE Yan,MURAD Ferid. Research progress on endothelial nitric oxide synthase uncoupling[J]. Chinese Pharmacological Bulletin, 2006, 22(6): 659-663 | |
| Authors: | ZHENG Jian-pu BIAN Ka KE Yan MURAD Ferid |
| Affiliation: | 1. Murad Research Institute for Modernized Chinese Medicine, Shanghai University of Traditional Chinese Medicine,Shanghai 201203, China ;2. E-Institnte of Shanghai Universities, Division of Nitric Oxide and Inflammatory Medicine. Shanghai 201203, China;3. Dept of Integrative Biology and Pharmacology, Institute of Molecular Medicine, University of Texas Medical School, 6431 Fannin, Houston, TX 77030 |
| Abstract: | Endothelial dysfunction in various vascular diseases is associated with reduced nitric oxide(NO) bioavailability.It has been clearly demonstrated that endothelial nitric oxide synthase(eNOS) uncoupling plays a key role in above vascular pathological status.eNOS uncoupling is characterized by eNOS generating super oxide rather than NO which may resulted from the increased oxidative stress,lack of eNOS protein cofactor tetrahydrobiopterin(BH4),or supplement shortage of eNOS substrate L-arginine.Accumulating evidences suggest that reversal of eNOS uncoupling by ether reduction of oxidative stress or promotion the bioavailability of BH4 and L-arginine may serve as a novel therapeutic strategy for endothelial dysfunction and cardiovascular diseases,such as hypertension,diabetes,and atherosclerosis. |
| Keywords: | eNOS uncoupling endothelial dysfunction nitric oxide oxidative stress tetrahydrobiopterin |
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