Status epilepticus does not induce acute brain inflammatory response in the Amazon rodent Proechimys, an animal model resistant to epileptogenesis

Scorza, Carla A.; Marques, Márcia Jonathas Guimarães; Silva, Sérgio Gomes da; Naffah‐Mazzacoratti, Maria da Graça; Scorza, Fúlvio A.; Cavalheiro, Ésper A.

doi:10.1016/j.neulet.2017.02.049

Cited by 32 publications

(16 citation statements)

References 32 publications

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“…In contrast, systemic treatment with Ac 2-26 reduced the IL-1β, IL-6 and GRO/KC levels, confirming its anti-inflammatory role as having been demonstrated in other experimental models of neuroinflammation and uveitis and ocular allergies [17, 18, 25, 26, 52]. Inflammation plays a crucial role in the generation of epileptic seizures, as demonstrated in an animal model resistant to epileptogenesis, the neotropical rodent Proechimys [53]. After systemic pilocarpine-induced SE, neotropical rodents showed no changes in IL-1β, IL-6, IL-10, TNF-α and VEGF levels in the hippocampus and cortex compared to the control group.…”

Section: Discussionmentioning

confidence: 56%

Annexin A1-derived peptide Ac2-26 in a pilocarpine-induced status epilepticus model: anti-inflammatory and neuroprotective effects

Gimenes

Andrade

Pinotti

et al. 2019

J Neuroinflammation

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BackgroundThe inflammatory process has been described as a crucial mechanism in the pathophysiology of temporal lobe epilepsy. The anti-inflammatory protein annexin A1 (ANXA1) represents an interesting target in the regulation of neuroinflammation through the inhibition of leukocyte transmigration and the release of proinflammatory mediators. In this study, the role of the ANXA1-derived peptide Ac2-26 in an experimental model of status epilepticus (SE) was evaluated.MethodsMale Wistar rats were divided into Naive, Sham, SE and SE+Ac2-26 groups, and SE was induced by intrahippocampal injection of pilocarpine. In Sham animals, saline was applied into the hippocampus, and Naive rats were only handled. Three doses of Ac2-26 (1 mg/kg) were administered intraperitoneally (i.p.) after 2, 8 and 14 h of SE induction. Finally, 24 h after the experiment-onset, rats were euthanized for analyses of neuronal lesion and inflammation.ResultsPilocarpine induced generalised SE in all animals, causing neuronal damage, and systemic treatment with Ac2-26 decreased neuronal degeneration and albumin levels in the hippocampus. Also, both SE groups showed an intense influx of microglia, which was corroborated by high levels of ionised calcium binding adaptor molecule 1(Iba-1) and monocyte chemoattractant protein-1 (MCP-1) in the hippocampus. Ac2-26 reduced the astrocyte marker (glial fibrillary acidic protein; GFAP) levels, as well as interleukin-1β (IL-1β), interleukin-6 (IL-6) and growth-regulated alpha protein (GRO/KC). These effects of the peptide were associated with the modulation of the levels of formyl peptide receptor 2, a G-protein-coupled receptor that binds to Ac2-26, and the phosphorylated extracellular signal-regulated kinase (ERK) in the hippocampal neurons.ConclusionsThe data suggest a neuroprotective effect of Ac2-26 in the epileptogenic processes through downregulation of inflammatory mediators and neuronal loss.

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Section: Discussionmentioning

confidence: 56%

Annexin A1-derived peptide Ac2-26 in a pilocarpine-induced status epilepticus model: anti-inflammatory and neuroprotective effects

Gimenes

Andrade

Pinotti

et al. 2019

J Neuroinflammation

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“…On the other hand, no differences were observed in the number of CD68-positive cells (marker of monocytes/macrophages) or CD11b/c positive cells (marker of activated microglia) between vehicle-and atorvastatin-treated rats 6 weeks after electrically-induced status epilepticus [45]. The current results are particularly interesting considering that proinflammatory cytokines may play a role in epileptogenesis, since hippocampal and cortical levels of inflammatory cytokines (IL-1β, IL-6, IL-10, and TNF-α) are not altered after status epilepticus in the Amazon rodent Proechimys guyannensis, an animal species resistant to epileptogenesis [46]. Moreover, it has been demonstrated that omega-3 fatty acids, which reduce proinflammatory markers during epileptogenesis in rats subjected to the pilocarpine model of epilepsy, are promising disease-modifying agents for epilepsy [47].…”

Section: Discussionmentioning

confidence: 69%

Effect of atorvastatin on behavioral alterations and neuroinflammation during epileptogenesis

Oliveira

Grigoletto

Canzian

et al. 2018

Epilepsy & Behavior

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Temporal lobe epilepsy (TLE) is the most frequent and medically refractory type of epilepsy in humans. In addition to seizures, patients with TLE suffer from behavioral alterations and cognitive deficits. Poststatus epilepticus model of TLE induced by pilocarpine in rodents has enhanced the understanding of the processes leading to epilepsy and thus, of potential targets for antiepileptogenic therapies. Clinical and experimental evidence suggests that inflammatory processes in the brain may critically contribute to epileptogenesis. Statins are inhibitors of cholesterol synthesis, and present pleiotropic effects that include antiinflammatory properties. We aimed the present study to test the hypothesis that atorvastatin prevents behavioral alterations and proinflammatory state in the early period after pilocarpine-induced status epilepticus. Male and female C57BL/6 mice were subjected to status epilepticus induced by pilocarpine and treated with atorvastatin (10 or 100mg/kg) for 14days. Atorvastatin slightly improved the performance of mice in the open-field and object recognition tests. In addition, atorvastatin dose-dependently decreased basal and status epilepticus-induced levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (INF-γ) and increased interleukin-10 (IL-10) levels in the hippocampus and cerebral cortex. The antiinflammatory effects of atorvastatin were qualitatively identical in both sexes. Altogether, these findings extend the range of beneficial actions of atorvastatin and indicate that its antiinflammatory effects may be useful after an epileptogenic insult.

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“…In experimental models, upregulated expression of IL-1β was also detected in epileptogenic tissues from animals with epilepsy of different etiologies 44 , 45 . Studies showed that mRNA expression of IL-1β, VEGF, TNF-α and TGF-β1 was significantly upregulated in the hippocampus after seizures 46 – 48 . Ho et al demonstrated that peripheral inflammation induced by LPS could increase seizure susceptibility via upregulation of IL-1β, TNF-α and IL-6 49 ; Auvin et al found that IL-1β receptor antagonist could partially reverses the enhancement of epileptogenesis in immature rat brains 44 ; Xiao et al 50 reported that IL-1β level was associated with the epileptogenesis of mesial temporal lobe epilepsy, and the mechanism was that IL-1β might induce activation of mammalian target of rapamycin (mTOR), followed by activation of neurons, which was crucial for the pathogenesis of mesial temporal lobe epilepsy chronicity; Viviani et al found that IL-1β could upregulate NMDA receptors on postsynaptic cells through activating the GluN2B subunit of the NMDA receptor, which was associated with induction of seizures 16 ; Postnikova et al showed that expression of the GluN2B mRNA upregulated significantly at 24 h following seizures, which might result in impairment of synaptic plasticity 51 .…”

Section: Discussionmentioning

confidence: 99%

Association between IL-1β and recurrence after the first epileptic seizure in ischemic stroke patients

Zhang

Zhao

et al. 2020

Sci Rep

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To analyze the association of IL-1β with recurrence after the first epileptic seizure in ischemic stroke patients and evaluate its predictive value. 238 patients with the first epileptic seizure after ischemic stroke were included in this study. IL-1β expression levels were detected through quantitative Real-Time PCR. Kaplan–Meier method was used to perform univariate analysis with log-rank test. The variables with P < 0.1 were then included in multivariate analysis. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value. Among all 238 patients, 107 patients (44.96%) had seizure recurrence and 131 patients (55.04%) had no recurrence. Kaplan–Meier analysis showed that high expression of IL-1β, low age (< 65 years), male, cortical involvement, large lesion size, late onset, severe neurological impairment and partial seizure type were associated with seizure recurrence. Multivariate analysis showed that IL-1β expression level (hazard ratio 2.057, 95% confidence interval 1.296–3.318) was independently associated with seizure recurrence. The area under ROC curve (AUC) was 0.803 (SE 0.030, 95% confidence interval 0.744–0.862) when IL-1β expression levels were applied in predicting seizure recurrence. IL-1β might be a useful biomarker for early discovery of recurrence after the first epileptic seizure in ischemic stroke patients.

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Status epilepticus does not induce acute brain inflammatory response in the Amazon rodent Proechimys, an animal model resistant to epileptogenesis

Cited by 32 publications

References 32 publications

Annexin A1-derived peptide Ac2-26 in a pilocarpine-induced status epilepticus model: anti-inflammatory and neuroprotective effects

Annexin A1-derived peptide Ac2-26 in a pilocarpine-induced status epilepticus model: anti-inflammatory and neuroprotective effects

Effect of atorvastatin on behavioral alterations and neuroinflammation during epileptogenesis

Association between IL-1β and recurrence after the first epileptic seizure in ischemic stroke patients

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