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Seizures, antiepileptics, antioxidants and oxidative stress: an insight for researchers.

机译:癫痫发作,抗癫痫药,抗氧化剂和氧化应激:研究人员的见解。

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BACKGROUND: Neuronal hyperexcitability and excessive production of free radicals have been implicated in the pathogenesis of a considerable range of neurological disorders, including epilepsy. The high rate of oxidative metabolism, coupled with the low antioxidant defenses and the richness in polyunsaturated fatty acids, makes the brain highly vulnerable to free radical damage. The increased susceptibility of the brain to oxidative damage highlights the importance of understanding the role of oxidative stress in the pathophysiology of seizures. OBJECTIVES: The present review aims not only to address the link between mitochondrial dysfunction, oxidative stress and seizures, but also the modulation of the pro-oxidant/antioxidant balance following seizures and treatment with antioxidants and antiepileptic drugs. METHODS: A literature review revealed that there are articles that address the role of oxidative stress and mitochondrial dysfunction in neurological disorders, including those involving differentseizure models where the modulation of the pro-oxidant/antioxidant balance by seizures per se and by antioxidant agents is discussed. However, the critical role of oxidative stress in all seizure models is not uniform. Therefore, there is a need for a review article that will address all these issues together. RESULTS/CONCLUSIONS: The experimental and clinical data suggest a putative role of oxidative stress in the pathophysiology of certain seizure types. The pro-oxidant/antioxidant balance is not only modulated by seizures per se, but also by antiepileptic drugs. The ability of antioxidants for reducing the seizure manifestations and the accompanying biochemical changes (i.e., markers of oxidative stress) further supports a role of free radicals in seizures and highlights a possible role of antioxidants as adjuncts to antiepileptic drugs for better seizure control.
机译:背景:神经元过度兴奋和自由基的过度产生与包括癫痫在内的多种神经系统疾病的发病机制有关。高的氧化代谢率,再加上低的抗氧化防御能力和多不饱和脂肪酸的丰富性,使大脑极易受到自由基的损害。脑对氧化损伤的敏感性增加,突出了了解氧化应激在癫痫发作的病理生理中的作用的重要性。目的:本综述的目的不仅在于解决线粒体功能障碍,氧化应激和癫痫发作之间的联系,还在于癫痫发作以及用抗氧化剂和抗癫痫药治疗后调节促氧化剂/抗氧化剂平衡。方法:文献综述表明,有文章探讨了氧化应激和线粒体功能障碍在神经系统疾病中的作用,包括涉及不同癫痫发作模型的文章,其中讨论了癫痫发作本身和抗氧化剂对促氧化剂/抗氧化剂平衡的调节作用。 。但是,氧化应激在所有癫痫发作模型中的关键作用并不统一。因此,需要有一篇评论文章将一起解决所有这些问题。结果/结论:实验和临床数据表明氧化应激在某些癫痫发作类型的病理生理中具有假定的作用。促氧化剂/抗氧化剂的平衡不仅受到癫痫发作本身的调节,而且还受到抗癫痫药的调节。抗氧化剂减少癫痫发作表现和伴随的生化变化(即氧化应激的标志物)的能力进一步支持了自由基在癫痫发作中的作用,并强调了抗氧化剂作为抗癫痫药的辅助剂以更好地控制癫痫发作的可能作用。

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