Levetiracetam inhibits interleukin-1β inflammatory responses in the hippocampus and piriform cortex of epileptic rats

Kim, Jieun; Choi, Hojun; Song, Hong-Ki; Jo, Seung-Mook; Kim, Duk‐Soo; Choi, Soo‐Young; Kim, Yeong-In; Kang, Tae‐Cheon

doi:10.1016/j.neulet.2010.01.018

Cited by 64 publications

(52 citation statements)

References 22 publications

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“…Some of the underlying mechanisms observed in these studies include decreased expression of proinflammatory cytokines and TNF-a through inhibition of transcription factors, inhibition of leukocyte migration to the inflammation site and inhibition of the histone deacetylase system involved in the regulation of inflammatory gene expression, among a few more [28][29][30]. Similarly, levetiracetam contributed to a decrease in the expression of IL-1b system and reduced the reactive gliosis in the hippocampus and the pyriform cortex of rats with chronic epilepsy [31]. Both drugs are widely used early in the treatment of SE in adults and children, but whether these anti-inflammatory effects are also present in humans, and the degree to which they may contribute to the control of seizures in acute situations remains to be demonstrated.…”

Section: Anti-inflammatory Effects Of Classic Aedsmentioning

confidence: 98%

Autoimmunity and inflammation in status epilepticus: from concepts to therapies

Holzer

Seeck

Korff³

2014

Expert Review of Neurotherapeutics

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The understanding of immunological mechanisms underlying some forms of epilepsy and encephalitis has rapidly increased for the last 10 years leading to the concept of status epilepticus of autoimmune origin. Actual treatment recommendations regarding autoimmune status epilepticus are based on retrospective case studies, pathophysiological considerations and experts' opinion. In addition, there are no clear indicators to predict outcome. In situations where autoimmune mechanisms are suspected in patients with status epilepticus, there is evidence that earlier treatment is related to better outcome. Increased awareness is mandatory to decrease the number of patients with major neurological problems or fatal outcome, which is overall about 50%. We here summarize findings of all pediatric and adult patients reported to date, and review the current state of knowledge in the field of immune therapeutic approaches of status epilepticus.

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Section: Anti-inflammatory Effects Of Classic Aedsmentioning

confidence: 98%

Autoimmunity and inflammation in status epilepticus: from concepts to therapies

Holzer

Seeck

Korff³

2014

Expert Review of Neurotherapeutics

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“…The modulation of cytokine production by LTG, TPM and LEV has been subject to small exploratory studies, but not systematically in-vitro or in-vivo (Neuman et al, 2012;Kim et al, 2010;Koçer et al, 2009). Systematic investigation of the modulation of cytokine production by AEDs would clarify whether AEDs with mood stabilizing properties differ from AEDs without clear mood stabilizing effects.…”

Section: Introductionmentioning

confidence: 99%

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Himmerich¹,

Bartsch²,

Hamer³

et al. 2013

Journal of Psychiatric Research

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“…LEV had an anti-inflammatory effect against interleukin-1β (IL-1β) and prostaglandin E2 in animal models of epilepsy [5,6]. However, LEV showed only minor antiinflammatory effects that were not sufficient to ameliorate the disease course of experimental autoimmune encephalomyelitis [7].…”

Section: Discussionmentioning

confidence: 99%

Effects of antiepileptic drugs on microglial properties

Taguchi

Sakuma

Suzuki

et al. 2018

E&S

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Purpose:To elucidate the effects of antiepileptic dr ugs (AEDs) on micr oglial cytokine pr oduction, polarization, and morphology. Methods: MG6, an immor talized mouse micr oglial cell line, was stimulated with lipopolysaccharides (LPS) and the levels of pro-inflammatory cytokines were measured by enzyme linked immunosorbent assay, quantitative polymerase chain reaction (q-PCR), and intracellular staining using flow cytometry. M1 and M2 signatures of microglia after polarization were assessed using quantitative PCR and flow cytometry. Primary microglia prepared from CX3CR1-GFP mice were used to study the effects of AEDs on microglial morphology. Results: Valpr oic acid (VPA) or gabapentin (GBP) augmented LPS-induced interleukin-6 (IL -6) production, while phenobarbital (PB) suppressed it. Tumor necrosis factor α (TNFα) production was enhanced by VPA, but was suppressed by PB and GBP. Levetiracetam did not alter cytokine production. It was difficult to assess the effects of water-insoluble AEDs because dimethyl sulfoxide solvent markedly suppressed IL-6 production. The mechanism of altered IL-6 production by AEDs was independent of their transcription or extracellular release. VPA augmented microglial M1 polarization. AEDs did not substantially affect the expression of microglial surface markers and had limited effect on the morphology of primary microglia. Discussion: Although VPA incr eased micr oglial pr oduction of pr o-inflammatory cytokines, partly due to augmented M1 polarization, most of the AEDs tested in the present study had neither beneficial nor adverse effects on inflammation in clinical practice.

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Levetiracetam inhibits interleukin-1β inflammatory responses in the hippocampus and piriform cortex of epileptic rats

Cited by 64 publications

References 22 publications

Autoimmunity and inflammation in status epilepticus: from concepts to therapies

Autoimmunity and inflammation in status epilepticus: from concepts to therapies

Impact of mood stabilizers and antiepileptic drugs on cytokine production in-vitro

Effects of antiepileptic drugs on microglial properties

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