氧化应激与癫痫发作

Oxidative Stress and Epileptic Seizures

由过量自由基释放导致的氧化应激参与了多种神经退化性疾病的病理过程。然而,氧化应激和癫痫之间的关系最近才得到认可。积累的证据证明氧化应激作为一个关键因素不仅是癫痫发作的后果,而且可能参与了癫痫发生。因此,旨在降低氧化应激的抗氧化治疗最近在癫痫治疗中引起相当的关注。然而,许多资料表明在所有的癫痫发作模型中氧化应激的表现特征不尽相同。这篇综述回顾了不同的动物癫痫模型(比如,红藻氨酸、匹鲁卡品、戊四氮),急性和慢性氧化应激的产生和影响,认为它对蛋白、脂质和抗氧化防御系统产生危害,这篇综述并且分析了癫痫发作中氧化应激产生的可能原因。提示抗氧化治疗可能可以作为缓解癫痫发作和保护损伤神经元的方法。

Oxidative stress resulting from excessive free-radical release is involved in the pathogenesis of a number of neurologic conditions and neurodegenerative disorders. However, the role of oxidative stress in epilepsies has only recently begun to be recognized. Accumulative evidence shows that Oxidative stress is emerging as a key factor that not only resulted from seizures, but may also contribute to epileptogenesis. Therefore, antioxidant therapies aimed at reducing oxidative stress have received considerable attention in epilepsy treatment. However, much evidence suggests that oxidative stress does not always have the same pattern in all seizures models. Thus, this review provides an overview aimed at achieving a better understanding of this issue. Evidence for the production and consequences of acute and chronic oxidative stress in various animal models of epilepsy （i.e., genetic rat models, kainic acid, pilocarpine, pentylenetetrazol） are reviewed, and damage to proteins, lipids, and antioxidant defenses is considered. In addition, this article analyzed the causes of oxidative stress in epileptic seizures. This review suggests that antioxidant treatment may be a way to attenuate seizure and protect damage neurons.