The compelling role of allopurinol in hyperuricemia-induced epilepsy: Unrecognized like tears in rain

IF 3.5 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin Pub Date : 2024-05-07 DOI:10.1016/j.brainresbull.2024.110973

Ali Abdullah AlAseeri , Hayder M. Al-kuraishy , Ali I. Al-Gareeb , Naif H. Ali , Athanasios Alexiou , Marios Papadakis , Mostafa M. Bahaa , Mubarak Alruwaili , Gaber El-Saber Batiha

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Abstract

Epilepsy is a common neurological disease characterized by the recurrent, paroxysmal, and unprovoked seizures. It has been shown that hyperuricemia enhances and associated with the development and progression of epilepsy through induction of inflammation and oxidative stress. In addition, uric acid is released within the brain and contributes in the development of neuronal hyperexcitability and epileptic seizure. Brain uric acid acts as damage associated molecular pattern (DAMP) activates the immune response and induce the development of neuroinflammation. Therefore, inhibition of xanthine oxidase by allopurinol may reduce hyperuricemia-induced epileptic seizure and associated oxidative stress and inflammation. However, the underlying mechanism of allopurinol in the epilepsy was not fully elucidated. Therefore, this review aims to revise from published articles the link between hyperuricemia and epilepsy, and how allopurinol inhibits the development of epileptic seizure.

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别嘌醇在高尿酸血症诱发癫痫中的作用令人信服：像雨中的泪水一样不为人知。

癫痫是一种常见的神经系统疾病，其特点是反复发作、阵发性发作和无诱因发作。研究表明，高尿酸血症会诱发炎症和氧化应激，从而促进癫痫的发生和发展。此外，尿酸会在大脑中释放，导致神经元过度兴奋和癫痫发作。脑尿酸作为损伤相关分子模式（DAMP）激活免疫反应，诱发神经炎症的发展。因此，别嘌醇抑制黄嘌呤氧化酶可减少高尿酸血症诱发的癫痫发作以及相关的氧化应激和炎症反应。然而，别嘌醇在癫痫中的作用机制尚未完全阐明。因此，本综述旨在从已发表的文章中重新审视高尿酸血症与癫痫之间的联系，以及别嘌醇是如何抑制癫痫发作的。

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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来源期刊

Brain Research Bulletin 医学-神经科学

CiteScore

6.90

自引率

2.60%

发文量

253

审稿时长

67 days

期刊介绍： The Brain Research Bulletin (BRB) aims to publish novel work that advances our knowledge of molecular and cellular mechanisms that underlie neural network properties associated with behavior, cognition and other brain functions during neurodevelopment and in the adult. Although clinical research is out of the Journal''s scope, the BRB also aims to publish translation research that provides insight into biological mechanisms and processes associated with neurodegeneration mechanisms, neurological diseases and neuropsychiatric disorders. The Journal is especially interested in research using novel methodologies, such as optogenetics, multielectrode array recordings and life imaging in wild-type and genetically-modified animal models, with the goal to advance our understanding of how neurons, glia and networks function in vivo.

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