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一氧化氮合酶(NOS)合成的一氧化氮(NO)是调节血管舒张功能的重要因子。四氢生物蝶呤(BH4)是NOS的重要辅助因子。BH4在体内的稳定性由从头合成、补救合成、氧化消耗及再循环所决定。当BH4/NOS的比例失调,可导致NOS催化L-精氨酸的作用解耦联,NOS催化产物由NO变为超氧阴离子(O2-)。O2-能与NO反应生成氧化性很强的氧亚硝基(ONOO-),ONOO-能迅速氧化BH4,加剧NOS的解耦联。NOS解耦联是高血压病、糖尿病、动脉粥样硬化等疾病中内皮细胞功能障碍的重要原因,因而通过纠正NOS解耦联可有效改善内皮细胞功能,有望为保护血管内皮功能提供有效途径。
Nitric oxide (NO) synthesized by nitric oxide synthase (NOS) is an important factor in the regulation of vasodilation. Tetrahydrobiopterin (BH4) is an important cofactor for NOS. The in vivo stability of BH4 is determined by de novo synthesis, remedial synthesis, oxidative depletion and recycle. When the ratio of BH4 / NOS is imbalanced, NOS catalyzes the decoupling of L-arginine and the NOS catalytic product changes from NO to superoxide anion (O2-). O2- can react with NO to form highly oxidizable oxy-nitroso group (ONOO-). ONOO- can rapidly oxidize BH4 and aggravate the decoupling of NOS. NOS decoupling is an important cause of endothelial cell dysfunction in diseases such as hypertension, diabetes and atherosclerosis. Therefore, it is expected to provide an effective way to protect the endothelial function by correcting the effect of NOS decoupling on endothelial cell function.