摘要
癫痫病是最常见的严重神经系统疾病之一,全世界有七千万人受到影响。为了治疗癫痫,抗癫痫药(AED)和外科手术被广泛使用。然而,耐药性和不良反应表明需要在进一步探索癫痫发生机理的基础上开发靶向AED。当前,已经作出许多努力来阐明癫痫发生中的神经炎症理论,其可能显示出治疗癫痫的潜力。在这方面,重要的靶蛋白,高迁移率族盒1(HMGB1),受到越来越多的关注,并得到了迅速发展。 HMGB1在各种真核细胞中表达,并位于细胞核中。 HMGB1因受伤或疾病而释放时,会参与炎症反应。最近的研究表明,HMGB1通过Toll样受体(TLR)途径可以触发炎症反应,并在癫痫中起重要作用。另外,对HMGB1的研究显示了其在治疗癫痫中的潜力。本文中,作者分析了HMGB1-TLR途径在癫痫中的实验和临床证据,总结了癫痫发生的理论,并为这一新领域的抗癫痫治疗提供了见识。
关键词: 神经炎症,HMGB1,TLR,HMGB1-TLR途径,癫痫,抗癫痫药。
Current Drug Targets
Title:The Potential Therapeutic Role of the HMGB1-TLR Pathway in Epilepsy
Volume: 22 Issue: 2
关键词: 神经炎症,HMGB1,TLR,HMGB1-TLR途径,癫痫,抗癫痫药。
摘要: Epilepsy is one of the most common serious neurological disorders, affecting over 70 million people worldwide. For the treatment of epilepsy, antiepileptic drugs (AEDs) and surgeries are widely used. However, drug resistance and adverse effects indicate the need to develop targeted AEDs based on further exploration of the epileptogenic mechanism. Currently, many efforts have been made to elucidate the neuroinflammation theory in epileptogenesis, which may show potential in the treatment of epilepsy. In this respect, an important target protein, high mobility group box 1 (HMGB1), has received increased attention and has been developed rapidly. HMGB1 is expressed in various eukaryotic cells and localized in the cell nucleus. When HMGB1 is released by injuries or diseases, it participates in inflammation. Recent studies suggest that HMGB1 via Toll-like receptor (TLR) pathways can trigger inflammatory responses and play an important role in epilepsy. In addition, studies of HMGB1 have shown its potential in the treatment of epilepsy. Herein, the authors analyzed the experimental and clinical evidence of the HMGB1-TLR pathway in epilepsy to summarize the theory of epileptogenesis and provide insights into antiepileptic therapy in this novel field.
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The Potential Therapeutic Role of the HMGB1-TLR Pathway in Epilepsy, Current Drug Targets 2021; 22 (2) . https://dx.doi.org/10.2174/1389450121999200729150443
DOI https://dx.doi.org/10.2174/1389450121999200729150443 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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