Hensley K, Carney J M, Stewart C A, Tabatabaie T, Pye Q, Floyd R A
Oklahoma Medical Research Foundation, Department of Free Radical Biology and Aging, Oklahoma City, USA.
Int Rev Neurobiol. 1997;40:299-317. doi: 10.1016/s0074-7742(08)60725-4.
Nitrone-based spin trapping compounds have been shown to protect experimental animals from pathology associated with ischaemia/reperfusion injury, endotoxaemia, natural and accelerated aging, certain xenobiotics, and physical trauma. Moreover, these compounds have an intriguing nootropic action. Nitrones affect pathophysiological correlates in both the central nervous system and peripheral organ systems. These compounds have been shown to affect cellular oxidation state and oxidatively sensitive enzyme systems, but the precise mode of nitrone action has not been elucidated. Recent discoveries regarding the ability of nitrones to suppress gene transcriptional events associated with pathophysiological states, particularly the elaboration of NF kappa B-regulated cytokines and inducible nitric oxide synthase, argue that nitrones may act at a proximal level to oxidatively sensitive signal amplification systems.
基于硝酮的自旋捕获化合物已被证明能保护实验动物免受与缺血/再灌注损伤、内毒素血症、自然衰老和加速衰老、某些外源性物质以及物理创伤相关的病理影响。此外，这些化合物还具有引人关注的益智作用。硝酮会影响中枢神经系统和外周器官系统中的病理生理关联。这些化合物已被证明会影响细胞氧化状态和氧化敏感酶系统，但硝酮的确切作用模式尚未阐明。最近有关硝酮抑制与病理生理状态相关的基因转录事件的能力的发现，尤其是核因子κB调节的细胞因子和诱导型一氧化氮合酶的释放，表明硝酮可能在氧化敏感信号放大系统的近端起作用。
