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IL-1 receptor/Toll-like receptor signaling in infection, inflammation, stress and neurodegeneration couples hyperexcitability and seizures.IL-1 受体/ Toll 样受体信号在感染、炎症、应激和神经退行性变中与过度兴奋和癫痫发作有关。
Brain Behav Immun. 2011 Oct;25(7):1281-9. doi: 10.1016/j.bbi.2011.03.018. Epub 2011 Apr 5.
2
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.
3
Cox-2 inhibition can lead to adverse effects in a rat model for temporal lobe epilepsy.COX-2 抑制可导致颞叶癫痫大鼠模型出现不良反应。
Epilepsy Res. 2010 Sep;91(1):49-56. doi: 10.1016/j.eplepsyres.2010.06.011.
4
Inflammation induced by LPS enhances epileptogenesis in immature rat and may be partially reversed by IL1RA.内毒素诱导的炎症增强了未成熟大鼠的癫痫发生,IL1RA 可能部分逆转这一过程。
Epilepsia. 2010 Jul;51 Suppl 3(Suppl 3):34-8. doi: 10.1111/j.1528-1167.2010.02606.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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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
J Neurosci. 2010 Jun 2;30(22):7484-94. doi: 10.1523/JNEUROSCI.0551-10.2010.
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Targeting Toll-like receptors: emerging therapeutics?靶向 Toll 样受体:新兴治疗方法?
Nat Rev Drug Discov. 2010 Apr;9(4):293-307. doi: 10.1038/nrd3203.
8
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。
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Neuroprotection by selective allosteric potentiators of the EP2 prostaglandin receptor.选择性别构增强剂对 EP2 前列腺素受体的神经保护作用。
Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2307-12. doi: 10.1073/pnas.0909310107. Epub 2010 Jan 14.
10
ICE/caspase 1 inhibitors and IL-1beta receptor antagonists as potential therapeutics in epilepsy.ICE/半胱天冬酶1抑制剂和白细胞介素-1β受体拮抗剂作为癫痫的潜在治疗药物。
Curr Opin Investig Drugs. 2010 Jan;11(1):43-50.

介导炎症对癫痫影响的分子级联反应。

Molecular cascades that mediate the influence of inflammation on epilepsy.

机构信息

Department of Physiology and Neurobiology, Faculty of Health Sciences, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

出版信息

Epilepsia. 2011 May;52 Suppl 3(0 3):33-9. doi: 10.1111/j.1528-1167.2011.03034.x.

DOI:10.1111/j.1528-1167.2011.03034.x
PMID:21542844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3638118/
Abstract

Experimental evidence strongly indicates a significant role for inflammatory and immune mediators in initiation of seizures and epileptogenesis. Here we will summarize data supporting the involvement of IL-1β, TNF-α and toll-like receptor 4 in seizure generation and the process of epileptogenesis. The physiological homeostasis and control over brain immune response depends on the integrity of the blood-brain barrier, transforming growth factor (TGF)-β signaling and leukocyte migration. To what extent targeting the immune system is successful in preventing epileptogenesis, and which signaling pathway should be beleaguered is still under intensive research.

摘要

实验证据强烈表明,炎症和免疫介质在癫痫发作和癫痫发生的启动中起着重要作用。在这里,我们将总结支持 IL-1β、TNF-α 和 Toll 样受体 4 参与癫痫发作和癫痫发生过程的数据。生理内稳态和对大脑免疫反应的控制依赖于血脑屏障的完整性、转化生长因子 (TGF)-β 信号和白细胞迁移。在多大程度上靶向免疫系统可以成功预防癫痫发生,以及应该针对哪个信号通路进行研究,仍在深入研究中。