晚期糖基化产物可清除一氧化氮，并介导实验性糖尿病中内皮依赖性血管舒张功能障碍。
Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.
作者信息
Bucala R, Tracey K J, Cerami A
机构信息
Laboratory of Medical Biochemistry, Rockefeller University, New York 10021.
出版信息
J Clin Invest. 1991 Feb;87(2):432-8. doi: 10.1172/JCI115014.
Abstract
Nitric oxide (an endothelium-derived relaxing factor) induces smooth muscle relaxation and is an important mediator in the regulation of vascular tone. Advanced glycosylation end products, the glucose-derived moieties that form nonenzymatically and accumulate on long-lived tissue proteins, have been implicated in many of the complications of diabetes and normal aging. We demonstrate that advanced glycosylation products quench nitric oxide activity in vitro and in vivo. Acceleration of the advanced glycosylation process in vivo results in a time-dependent impairment in endothelium-dependent relaxation. Inhibition of advanced glycosylation with aminoguanidine prevents nitric oxide quenching, and ameliorates the vasodilatory impairment. These results implicate advanced glycosylation products as important modulators of nitric oxide activity and endothelium-dependent relaxation.
摘要
一氧化氮（一种内皮源性舒张因子）可诱导平滑肌舒张，是调节血管张力的重要介质。晚期糖基化终产物是由葡萄糖衍生而来的部分，通过非酶促反应形成并积聚在长寿组织蛋白上，与糖尿病和正常衰老的许多并发症有关。我们证明，晚期糖基化产物在体外和体内均可淬灭一氧化氮活性。体内晚期糖基化过程的加速会导致内皮依赖性舒张功能随时间受损。用氨基胍抑制晚期糖基化可防止一氧化氮淬灭，并改善血管舒张功能障碍。这些结果表明晚期糖基化产物是一氧化氮活性和内皮依赖性舒张的重要调节因子。
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