Abstract：
Excessively high or synchronized neuronal activity in the brain is the underlying cause of epilepsy, a condition of the central nervous system. Epilepsy is caused mostly by an imbalance in the activity of inhibitory and excitatory neural networks. Recurrent or prolonged seizures lead to neuronal death, which in turn promotes epileptogenesis and epileptic seizures. Ferrous ion-mediated cell death is known as ferroptosis, which is due to the accumulation of lipid peroxidation products resulting from compromise of the glutathione (GSH)-dependent antioxidant system. The pathophysiology of epilepsy has been linked to anomalies in the glutathione peroxidase 4 (GPX4)/GSH redox pathway, lipid peroxidation, and iron metabolism. Studies have shown that inhibiting ferroptosis may alleviate cognitive impairment and decrease seizures, indicating that it is neuroprotective. With the hope of aiding the development of more novel approaches for the management of epilepsy, this research aimed to examine the role of ferroptosis in this disease.
摘要：
大脑中过高或同步的神经元活动是癫痫的根本原因，中枢神经系统的状况。癫痫主要是由抑制性和兴奋性神经网络活动的不平衡引起的。反复或长时间的癫痫发作导致神经元死亡，进而促进癫痫发生和癫痫发作。亚铁离子介导的细胞死亡被称为铁凋亡，这是由于谷胱甘肽（GSH）依赖性抗氧化系统受损导致的脂质过氧化产物的积累。癫痫的病理生理学与谷胱甘肽过氧化物酶4（GPX4）/GSH氧化还原途径的异常有关，脂质过氧化，和铁代谢。研究表明，抑制铁性凋亡可以减轻认知障碍和减少癫痫发作，表明它具有神经保护作用。希望帮助开发更新颖的治疗癫痫的方法，这项研究的目的是研究铁死亡在这种疾病中的作用。
