Efecto de los antioxidantes en la epilepsia del lóbulo temporal

e-CUCBA Pub Date : 2022-04-26 DOI:10.32870/ecucba.vi18.252
Kenia Pardo-Peña, Salvador M. Martínez-Gallegos, Marco A. Noriega-Ruiz
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Abstract

Epilepsy is a common neurological disorder that affects around 70 million people in the world, which represents approximately 1%of the world population. Seizures are transitory episodes produced by excessive neuronal discharges. They are characterized bytransient behavioral changes that are caused by abnormal and excessive neuronal synchronization in the brain. These episodes canbe triggered by genetic or acquired factors that alter normal brain function such as autoimmune diseases, genetic mutations,encephalopathies, head trauma, cerebrovascular accidents, febrile seizures or statusepilepticus. Temporal lobe epilepsy is a seriousneurological disorder, which represents 60% to 70% of drug-resistant epilepsy, and is an important form of epilepsy acquired byany of the factors mentioned. Seizures can generate recurrent cycles of excitotoxicity and oxidative stress that cause neuronaldamage and cell death. Oxidative stress is an imbalance between the endogenous antioxidant system and the overproduction ofreactive oxygen species (ROS), consequently, oxidation of proteins, lipids and nucleic acids occurs in the brain, resulting inapoptosis, proteopathies, mitochondrial dysfunction, glial cell activation and neuroinflammation. ROS are responsible for thegeneration of oxidative stress and could be involved in neuronal damage that contributes to the establishment of epileptogenesis andspontaneous seizures in patients and experimental models. The administration of agents with antioxidant and anti-inflammatoryproperties could represent a therapeutic alternative aimed at reducing oxidative stress during epileptogenesis or seizures to reducethe severity of the pathological processes involved, and thus attenuate the neurobiological consequences that occur in temporal lobeepilepsy.
抗氧化剂对颞叶癫痫的影响
癫痫是一种常见的神经系统疾病,影响着世界上约7000万人,约占世界人口的1%。癫痫发作是由过多的神经元放电引起的短暂发作。它们的特征是由大脑中异常和过度的神经元同步引起的短暂行为改变。这些发作可由改变正常脑功能的遗传或获得性因素引发,如自身免疫性疾病、基因突变、脑病、头部创伤、脑血管意外、发热性癫痫发作或癫痫持续状态。颞叶癫痫是一种严重的神经系统疾病,占耐药性癫痫的60%至70%,是由上述任何因素获得的癫痫的重要形式。癫痫发作可产生反复循环的兴奋性毒性和氧化应激,导致神经元损伤和细胞死亡。氧化应激是内源性抗氧化系统与活性氧(ROS)过量产生之间的不平衡,因此,大脑中发生蛋白质、脂质和核酸的氧化,导致细胞凋亡、蛋白质病变、线粒体功能障碍、胶质细胞活化和神经炎症。ROS负责氧化应激的产生,并可能参与神经元损伤,从而有助于患者和实验模型中癫痫发生和自发癫痫发作的建立。具有抗氧化和抗炎特性的药物可以作为一种治疗选择,旨在减少癫痫发生或癫痫发作期间的氧化应激,以减轻所涉及的病理过程的严重程度,从而减轻颞叶癫痫中发生的神经生物学后果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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