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炎症在癫痫中的作用。

The role of inflammation in epilepsy.

机构信息

Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via Giuseppe La Masa 19, 20156 Milan, Italy.

出版信息

Nat Rev Neurol. 2011 Jan;7(1):31-40. doi: 10.1038/nrneurol.2010.178. Epub 2010 Dec 7.

DOI:10.1038/nrneurol.2010.178
PMID:21135885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3378051/
Abstract

Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.

摘要

癫痫是第三大常见的慢性脑部疾病,其特征是存在持久的发作倾向。尽管在癫痫的药物治疗和手术治疗方面取得了进展,但对于导致个体发作的过程以及使健康大脑变得癫痫的机制,我们知之甚少。这些知识上的差距阻碍了更好的预防治疗和治愈方法的发展,因为大约 30%的癫痫病例对目前的治疗方法有抗药性。在这里,我们重点介绍越来越多的证据,这些证据支持炎症介质(由脑细胞和外周免疫细胞释放)在个体发作和致痫过程中的参与。我们首先描述了大脑炎症和免疫的各个方面,然后探讨了临床和实验研究中炎症与癫痫之间关系的证据。随后,我们讨论了癫痫发作如何引起炎症,以及这种炎症是否反过来影响癫痫发作的发生和严重程度以及与癫痫发作相关的神经元死亡。进一步深入了解炎症在癫痫发作和恶化中的复杂作用,应该为抗癫痫药物的设计提供新的分子靶点,这些药物不仅可以抑制这种疾病的症状,还可以预防或消除疾病的发病机制。

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1
The role of inflammation in epilepsy.炎症在癫痫中的作用。
Nat Rev Neurol. 2011 Jan;7(1):31-40. doi: 10.1038/nrneurol.2010.178. Epub 2010 Dec 7.
2
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本文引用的文献

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Infantile spasms: a U.S. consensus report.婴儿痉挛症:美国共识报告。
Epilepsia. 2010 Oct;51(10):2175-89. doi: 10.1111/j.1528-1167.2010.02657.x.
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Inflammation enhances epileptogenesis in the developing rat brain.炎症增强发育中大鼠大脑的癫痫发生。
Neurobiol Dis. 2010 Oct;40(1):303-10. doi: 10.1016/j.nbd.2010.06.004. Epub 2010 Jun 19.
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Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury.血脑屏障破坏作为创伤性脑损伤的治疗靶点。
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[Multiple comorbidities with migraine-Is there a common cause?].[偏头痛的多种合并症——是否存在共同病因?]
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Selective inhibition of NOX2 after status epilepticus attenuates epileptogenesis and cognitive impairment: A sex-dependent study.癫痫持续状态后对NOX2的选择性抑制可减轻癫痫发生和认知障碍:一项性别依赖性研究。
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Animal Models for the Study of Neurological Diseases and Their Link to Sleep.用于研究神经疾病及其与睡眠关系的动物模型
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Comparative Analysis of Systemic Inflammatory Biomarkers Across Multiple Antiseizure Medications: A Single-Center Retrospective Cohort Study of 1782 Patients.多种抗癫痫药物全身炎症生物标志物的比较分析:一项对1782例患者的单中心回顾性队列研究。
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Investigating biomarkers for personality alterations in temporal lobe epilepsy patients: based on peripheral inflammatory indices, electroencephalography, and neuroimaging.探究颞叶癫痫患者人格改变的生物标志物:基于外周炎症指标、脑电图和神经影像学
Front Psychiatry. 2025 Jul 28;16:1622726. doi: 10.3389/fpsyt.2025.1622726. eCollection 2025.
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Inflammatory Drug-Resistant Epilepsy Index (IDREI) as a Molecular Compound Biomarker in Focal Epilepsies.炎症性耐药癫痫指数(IDREI)作为局灶性癫痫的一种分子复合生物标志物
Biomolecules. 2025 Jun 22;15(7):914. doi: 10.3390/biom15070914.
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Mitochondrial dysfunction and NLRP3 inflammasome activation in drug-resistant epilepsy: emerging insights and mitochondrial-targeted therapeutic strategies.耐药性癫痫中的线粒体功能障碍与NLRP3炎性小体激活:新见解及线粒体靶向治疗策略
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jul 23. doi: 10.1007/s00210-025-04468-2.
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The emerging role for chemokines in epilepsy.趋化因子在癫痫中的新作用。
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Early life activation of toll-like receptor 4 reprograms neural anti-inflammatory pathways.早期生命中 Toll 样受体 4 的激活会重新编程神经抗炎途径。
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Systemic inflammatory cells fight off neurodegenerative disease.系统性炎症细胞能抵御神经退行性疾病。
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Epileptogenesis provoked by prolonged experimental febrile seizures: mechanisms and biomarkers.热性惊厥持续状态诱发的癫痫发生机制及生物标志物
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Trafficking of immune cells in the central nervous system.免疫细胞在中枢神经系统中的迁移。
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The COX-2 inhibitor parecoxib is neuroprotective but not antiepileptogenic in the pilocarpine model of temporal lobe epilepsy.环氧合酶-2 抑制剂帕瑞昔布具有神经保护作用,但不能预防匹罗卡品诱导的颞叶癫痫发作。
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Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures.Toll 样受体 4 和高迁移率族蛋白 1 参与了癫痫发作的发生机制,并且可以作为靶点来减少癫痫发作。
Nat Med. 2010 Apr;16(4):413-9. doi: 10.1038/nm.2127. Epub 2010 Mar 28.