The role of interleukin-1β in the pentylenetetrazole-induced kindling of seizures, in the rat hippocampus

Kołosowska, Karolina; Maciejak, Piotr; Szyndler, Janusz; Turzyńska, Danuta; Sobolewska, Alicja; Płaźnik, Adam

doi:10.1016/j.ejphar.2014.03.008

Cited by 28 publications

(14 citation statements)

References 47 publications

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“…These data supports that SE induced in the developing rat promotes a microenvironment that might favor neuronal cell death in the hippocampus and that may includes the acute and transient expression of IL-1β and IL-1RI, as shown here and by others (Rizzi et al 2003, Ravizza et al 2005, Järvelä et al 2011, Omran et al 2012, Kołosowska, et al 2014, glia activation (Rizzi et al 2003), augmented expression of other inflammatory cytokines (Rizzi et al 2003, Ravizza et al 2005, Järvelä et al 2011) and increased hippocampal excitability (Naylor et al 2013). IL-1β could interact with IL-1RI and trigger the extrinsic pathway of cell death resulting in necrotic neuronal cell death in the CA1 area.…”

Section: Discussionsupporting

confidence: 90%

“…However, additional doublelabelling experiments are necessary to confirm the phenotype of this IR cells. A similar increase in the number of IL-1RI IR cells was observed in DG granule layer after fully kindled seizures in adult rats (Kołosowska et al 2014). Then, this evidence shows that hippocampal expression of IL-1RI is susceptible to be modifi ed by seizures in both immature and adult brains, which in turn can mediate the physiological effects of IL-1β.…”

Section: Discussionsupporting

confidence: 67%

“…Recently, it has been shown that hippocampal concentration of IL-1β is augmented in adult rats after pentylentetrazole-induced chemical kindling; this effect is associated with an increase in the number of IL-1RI immunoreactive cells in dentate gyrus (Kołosowska et al 2014).…”

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confidence: 98%

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Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

Álvarez‐Croda

Santiago‐García

Medel-Matus

et al. 2016

An. Acad. Bras. Ciênc.

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The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteendays-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohistochemical procedures; Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. IL-1β mRNA expression was increased 6 h following SE, but not at 24 h; however IL-1RI mRNA expression was unaffected when comparing with the control group. IL-1β and IL-1RI immunoreactivity was not detected in control animals. IL-1β and IL-1RI were expressed in the CA1 pyramidal layer, the dentate gyrus granular layer and the hilus 6 h after SE, whereas injured cells were detected 24 h following seizures. Early expression of IL-1β and IL-1RI in the hippocampus could be associated with SE-induced neuronal cell death mechanisms in the developing rat.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 67%

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Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

Álvarez‐Croda

Santiago‐García

Medel-Matus

et al. 2016

An. Acad. Bras. Ciênc.

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“…The possibility that inflammatory processes in the brain contribute to seizures and the establishment of a chronic epileptic foci, is becoming increasingly recognized. Pro-inflammatory cytokines, including interleukin-1β, and danger signals, including HMGB1 and S100β, are overexpressed in human and experimental epileptogenic tissues ( 30 – 32 ). They have proconvulsant activity in various seizure models, possibly by reducing the seizure threshold via functional interactions with classical neurotransmitter systems ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

HMGB1 regulates P-glycoprotein expression in status epilepticus rat brains via the RAGE/NF-κB signaling pathway

Xie

Chen

et al. 2017

Molecular Medicine Reports

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Overexpression of P-glycoprotein (P-gp) in the brain is an important mechanism involved in drug-resistant epilepsy (DRE). High-mobility group box 1 (HMGB1), an inflammatory cytokine, significantly increases following seizures and may be involved in upregulation of P-gp. However, the underlying mechanisms remain elusive. The aim of the present study was to evaluate the role of HMGB1 and its downstream signaling components, receptor for advanced glycation end-product (RAGE) and nuclear factor-κB (NF-κB), on P-gp expression in rat brains during status epilepticus (SE). Small interfering RNA (siRNA) was administered to rats prior to induction of SE by pilocarpine, to block transcription of the genes encoding HMGB1 and RAGE, respectively. An inhibitor of NF-κB, pyrrolidinedithiocarbamic acid (PDTC), was utilized to inhibit activation of NF-κB. The expression levels of HMGB1, RAGE, phosphorylated-NF-κB p65 (p-p65) and P-gp were detected by western blotting. The relative mRNA expression levels of the genes encoding these proteins were measured using reverse transcription-quantitative polymerase chain reaction and the cellular localization of the proteins was determined by immunofluorescence. Pre-treatment with HMGB1 siRNA reduced the expression levels of RAGE, p-p65 and P-gp. PDTC reduced the expression levels of P-gp. These findings suggested that overexpression of P-gp during seizures may be regulated by HMGB1 via the RAGE/NF-κB signaling pathway, and may be a novel target for treating DRE.

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“…Previous experimental work, which has been conducted in animal models suggested that induction of seizures elicited by either various chemical agents ( Kaur et al, 2014 ; Kołosowska et al, 2014 ) or repeated electrical stimulation such as ECS ( Cardoso et al, 2011 ; Rothan et al, 2017 ) will ultimately lead to progressive development of seizures. Despite the development of new treatment approaches that have made great advances in the control of seizures, intolerable side effects of currently available treatments still pose a significant problem ( Amhaoul et al, 2014 ; Moshé et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Brain Lipopolysaccharide Preconditioning-Induced Gene Reprogramming Mediates a Tolerance State in Electroconvulsive Shock Model of Epilepsy

et al. 2018

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There is increasing evidence pointing toward the role of inflammatory processes in epileptic seizures, and reciprocally, prolonged seizures induce more inflammation in the brain. In this regard, effective strategies to control epilepsy resulting from neuroinflammation could be targeted. Based on the available data, preconditioning (PC) with low dose lipopolysaccharide (LPS) through the regulation of the TLR4 signaling pathway provides neuroprotection against subsequent challenge with injury in the brain. To test this, we examined the effects of a single and chronic brain LPS PC, which is expected to lead to reduction of inflammation against epileptic seizures induced by electroconvulsive shock (ECS). A total of 60 male Sprague Dawley rats were randomly assigned to five groups: control, vehicle (single and chronic), and LPS PC (single and chronic). We first recorded the data regarding the behavioral and histological changes. We further investigated the alterations of gene and protein expression of important mediators in relation to TLR4 and inflammatory signaling pathways. Interestingly, significant increased presence of NFκB inhibitors [Src homology 2-containing inositol phosphatase-1 (SHIP1) and Toll interacting protein (TOLLIP)] was observed in LPS-preconditioned animals. This result was also associated with over-expression of IRF3 activity and anti-inflammatory markers, along with down-regulation of pro-inflammatory mediators. Summarizing, the analysis revealed that PC with LPS prior to seizure induction may have a neuroprotective effect possibly by reprogramming the signaling response to injury.

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The role of interleukin-1β in the pentylenetetrazole-induced kindling of seizures, in the rat hippocampus

Cited by 28 publications

References 47 publications

Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

HMGB1 regulates P-glycoprotein expression in status epilepticus rat brains via the RAGE/NF-κB signaling pathway

Brain Lipopolysaccharide Preconditioning-Induced Gene Reprogramming Mediates a Tolerance State in Electroconvulsive Shock Model of Epilepsy

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