Prevention of pentylenetetrazole-induced kindling and behavioral comorbidities in mice by levetiracetam combined with the GLP-1 agonist liraglutide: Involvement of brain antioxidant and BDNF upregulating properties

Souza, Alana Gomes de; Filho, Adriano José Maia Chaves; Oliveira, João Almir; Souza, Denia Alves Albuquerque de; Lopes, Iardja Stéfane; Carvalho, Michelle Garcêz de; Lima, Klistenes Alves de; Sousa, Francisca Cléa Florenço de; Vasconcelos, Silvânia Maria Mendes; Macedo, Danielle; Fonteles, Marta Maria de França

doi:10.1016/j.biopha.2018.10.066

Cited by 61 publications

(19 citation statements)

References 72 publications

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“…50 Moreover, PTZ-induced kindling markedly increased nitrite levels in different brain areas. 51 Consistent with these observations, our study demonstrated that iNOS protein expression was increased and subsequently the production of NO was elevated in the brain of PTZ-kindled mice. Herein, we showed that treatment of PTZ-kindled mice with SIM significantly attenuated this increase in iNOS protein expression and brain NO level.…”

Section: Discussionsupporting

confidence: 87%

“…Distortion of NO homeostasis through iNOS upregulation is a leading cause of kainic acid‐mediated excitotoxicity in rat hippocampus 50 . Moreover, PTZ‐induced kindling markedly increased nitrite levels in different brain areas 51 . Consistent with these observations, our study demonstrated that iNOS protein expression was increased and subsequently the production of NO was elevated in the brain of PTZ‐kindled mice.…”

Section: Discussionsupporting

confidence: 85%

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Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Ahmed

Kamel

2020

Basic Clin Pharma Tox

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Cognitive impairments are frequently observed in epileptic patients, particularly in memory function. 1 Pentylenetetrazole (PTZ) kindling is generally accepted as a chronic experimental animal model of epilepsy. PTZ kindling causes modifications in the molecular and cellular levels, which are responsible for the oxidative stress and neurodegenerative changes in hippocampus 2 and lead to memory dysfunction. 3 Reactive aldehydes, including malondialdehyde (MDA) and 4-hydroxynonena (4-HNE), are the product of lipid peroxidation. The accumulation of such reactive aldehydes not only led to oxidative stress and neuronal death 4 but also resulted in a deterioration of

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 85%

Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Ahmed

Kamel

2020

Basic Clin Pharma Tox

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“…We can, therefore, assume that the long‐term treatment of Chrysin NPs improves epileptic disorders by can oxidative stress. [ 28,29 ]…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

Zhang¹,

Zhao

Afzal

et al. 2020

J Biochem & Molecular Tox

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Chrysin is the major bioactive compound of blue passionflower, an important medicinal plant used in traditional herbal formulations since ancient times. In the present study, we report that chrysin nanoparticles (chrysin NPs) protect Wistar rats against kindling‐induced epilepsy. Nanoparticles of sizes less than 150 nm with a spherical shape were prepared using poly(d,l‐lactic‐co‐glycolic acid) and polyvinyl alcohol, respectively, as polymer and stabilizer. Rats were injected with subconvulsive doses of pentylenetetrazole (PTZ) (35 mg/kg, intraperitoneal) every second day, with 22 injections in total, and on the same days, they received protective doses of the chrysin NPs (5 and 10 µg/mL, PO), respectively, 45 min before each PTZ injection. After the last PTZ injection, an average of thirteen seizure scores was recorded. Animals were killed by decapitation 24 h after a seizure. The cortex and hippocampus were removed and stored in liquid nitrogen for determining oxidative stress terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, histopathology, and reverse transcription‐polymerase chain reaction for messenger RNA expression. The result showed chrysin NPs treatment has counteracted oxidative stress, reduced neuronal apoptosis, and upregulated nuclear factor erythroid 2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), and NAD(P)H quinone oxidoreductase 1. In conclusion, our findings demonstrate that the neuroprotective effect of chrysin NPs against kindling‐induced epilepsy might be escorted by the alleviation of oxidative stress through the Nrf2/antioxidant response element/HO‐1 pathway signal pathway.

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“…GLP-1 analogues can regulate mTOR expression via the AMPactivated protein kinase (AMPK) pathway (He et al, 2016;Zhang et al, 2017). Although several studies have shown the anticonvulsant potential of GLP-1 analogues (Koshal and Kumar, 2016;Wang et al, 2018;de Souza et al, 2019), the effect of liraglutide on the epileptogenesis and cognitive dysfunction in the DS mouse model has not been examined. In the present study, we investigated the possible anti-epileptic effect of liraglutide in Scn1a KO-induced epileptic mice and its potential effect on both Bcl-2 regulate apoptotic pathway and the mTOR pathway that are involved in epileptogenesis.…”

Section: Introductionmentioning

confidence: 99%

The Glucagon-Like Peptide-1 Analogue Liraglutide Reduces Seizures Susceptibility, Cognition Dysfunction and Neuronal Apoptosis in a Mouse Model of Dravet Syndrome

et al. 2020

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Moreover, liraglutide protected against Scn1a KO-induced apoptosis, which was manifested in the phosphorylation of mTOR (KO+NS: 1.99 ± 0.31 vs. KO+Lira: 0.97 ± 0.18, P = 0.0004), as well as the downregulation of cleaved caspase-3 (KO+NS: 0.49 ± 0.04 vs. KO+Lira: 0.30 ± 0.01, P = 0.0003) and restoration of the imbalance between BAX (KO+NS: 0.90 ± 0.02 vs. KO +Lira: 0.75 ± 0.04, P = 0.0005) and BCL-2 (KO+NS: 0.46 ± 0.02 vs. KO+Lira: 0.61 ± 0.02, P = 0.0006). Collectively, these results show that liraglutide reduces seizure susceptibility and cognitive dysfunction in the mouse model of Dravet syndrome, and exerts anti-apoptotic and neuroprotective effects in Scn1a KO mice and cells.

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Prevention of pentylenetetrazole-induced kindling and behavioral comorbidities in mice by levetiracetam combined with the GLP-1 agonist liraglutide: Involvement of brain antioxidant and BDNF upregulating properties

Cited by 61 publications

References 72 publications

Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

The Glucagon-Like Peptide-1 Analogue Liraglutide Reduces Seizures Susceptibility, Cognition Dysfunction and Neuronal Apoptosis in a Mouse Model of Dravet Syndrome

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Prevention of pentylenetetrazole-induced kindling and behavioral comorbidities in mice by levetiracetam combined with the GLP-1 agonist liraglutide: Involvement of brain antioxidant and BDNF upregulating properties

Cited by 61 publications

References 72 publications

Involvement of H2S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Involvement of H2S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Neuroprotective role of chrysin‐loaded poly(lactic‐co‐glycolic acid) nanoparticle against kindling‐induced epilepsy through Nrf2/ARE/HO‐1 pathway

The Glucagon-Like Peptide-1 Analogue Liraglutide Reduces Seizures Susceptibility, Cognition Dysfunction and Neuronal Apoptosis in a Mouse Model of Dravet Syndrome

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Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice

Involvement of H₂S, NO and BDNF‐TrkB signalling pathway in the protective effects of simvastatin against pentylenetetrazole‐induced kindling and cognitive impairments in mice