Role of Inflammatory Mediators in the Pathogenesis of Epilepsy

被引：129

作者：

Shimada, Tadayuki ^{[1
]}

Takemiya, Takako ^{[2
]}

Sugiura, Hiroko ^{[1
]}

Yamagata, Kanato ^{[1
]}

机构：

[1] Tokyo Metropolitan Inst Med Sci, Neural Plast Project, Setagaya Ku, Tokyo 1568506, Japan

[2] Tokyo Womens Med Univ, Med Res Inst, Shinjuku Ku, Tokyo 1628666, Japan

来源：

MEDIATORS OF INFLAMMATION | 2014年 / 2014卷

关键词：

PROSTAGLANDIN-E SYNTHASE-1; IL-1 RECEPTOR ANTAGONIST; CENTRAL-NERVOUS-SYSTEM; ACID-INDUCED SEIZURE; MOBILITY GROUP BOX-1; KAINIC ACID; BRAIN INFLAMMATION; TNF-ALPHA; PILOCARPINE MODEL; RAT HIPPOCAMPUS;

D O I：

10.1155/2014/901902

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Epilepsy is one of the most common chronic brain disorders worldwide, affecting 1% of people across different ages and backgrounds. Epilepsy is defined as the sporadic occurrence of spontaneous recurrent seizures. Accumulating preclinical and clinical evidence suggest that there is a positive feedback cycle between epileptogenesis and brain inflammation. Epileptic seizures increase key inflammatory mediators, which in turn cause secondary damage to the brain and increase the likelihood of recurrent seizures. Cytokines and prostaglandins are well-known inflammatory mediators in the brain, and their biosynthesis is enhanced following seizures. Such inflammatory mediators could be therapeutic targets for the development of new antiepileptic drugs. In this review, we discuss the roles of inflammatory mediators in epileptogenesis.

引用

页数：8

共 80 条

[1] Gene expression profile in temporal lobe epilepsy [J].

Aronica, Eleonora ;

Gorter, Jan A. .

NEUROSCIENTIST, 2007, 13 (02) :100-108

[2] Inflammation induced by LPS enhances epileptogenesis in immature rat and may be partially reversed by IL1RA [J].

Auvin, Stephane ;

Shin, Don ;

Mazarati, Andrey ;

Sankar, Raman .

EPILEPSIA, 2010, 51 :34-38

[3] Cyclooxygenase-2 selective inhibitors aggravate kainic acid induced seizure and neuronal cell death in the hippocampus [J].

Baik, EJ ;

Kim, EJ ;

Lee, SH ;

Moon, CH .

BRAIN RESEARCH, 1999, 843 (1-2) :118-129

[4] CXCR4-activated astrocyte glutamate release via TNFa: amplification by microglia triggers neurotoxicity [J].

Bezzi, P ;

Domercq, M ;

Brambilla, L ;

Galli, R ;

Schols, D ;

De Clercq, E ;

Vescovi, A ;

Bagetta, G ;

Kollias, G ;

Meldolesi, J ;

Volterra, A .

NATURE NEUROSCIENCE, 2001, 4 (07) :702-710

[5] NEUROLOGIC DISEASE INDUCED IN TRANSGENIC MICE BY CEREBRAL OVEREXPRESSION OF INTERLEUKIN-6 [J].

CAMPBELL, IL ;

ABRAHAM, CR ;

MASLIAH, E ;

KEMPER, P ;

INGLIS, JD ;

OLDSTONE, MBA ;

MUCKE, L .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (21) :10061-10065

[6] Microglial inhibition of neuroprotection by antagonists of the EP1 prostaglandin E2 receptor [J].

Carlson, Noel G. ;

Rojas, Monica A. ;

Black, John-David ;

Redd, Jonathan W. ;

Hille, John ;

Hill, Kenneth E. ;

Rose, John W. .

JOURNAL OF NEUROINFLAMMATION, 2009, 6

[7] Endogenous PGE2 regulates membrane excitability and synaptic transmission in hippocampal CA1 pyramidal neurons [J].

Chen, C ;

Bazan, NG .

JOURNAL OF NEUROPHYSIOLOGY, 2005, 93 (02) :929-941

[8] Seizure susceptibility in immature brain due to lack of COX-2-induced PGF2α [J].

Chung, Jee-In ;

Kim, A. Young ;

Lee, Soo Hwan ;

Baik, Eun Joo .

EXPERIMENTAL NEUROLOGY, 2013, 249 :95-103

[9] Pharmacology of celecoxib in rat brain after kainate administration [J].

Ciceri, P ;

Zhang, Y ;

Shaffer, AF ;

Leahy, KM ;

Woerner, MB ;

Smith, WG ;

Seibert, K ;

Isakson, PC .

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2002, 302 (03) :846-852

[10] Therapeutic targets in prostaglandin E2 signaling for neurologic disease [J].

Cimino, P. J. ;

Keene, C. Dirk ;

Breyer, Richard M. ;

Montine, Kathleen S. ;

Montine, Thomas J. .

CURRENT MEDICINAL CHEMISTRY, 2008, 15 (19) :1863-1869

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