Neuroprotective mechanisms of sildenafil and selenium in PTZ-kindling model: Implications in epilepsy

Tawfik, Karim M.; Moustafa, Yasser M.; El-Azab, Mona F.

doi:10.1016/j.ejphar.2018.05.035

Cited by 42 publications

(25 citation statements)

References 77 publications

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“…In this study, seizure severity consistently increased in rats treated with PTZ, which is in accordance with the results of earlier studies [17,18].…”

Section: Discussionsupporting

confidence: 93%

Mild foot electrical stimulation is comparable with phenytoin in inhibiting pentylenetetrazol-induced kindling in rats

et al. 2019

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Increasing evidence demonstrates that electric stimulation has anticonvulsant effects. The present study was undertaken to investigate the effects of mild foot electrical stimulation (MFES) on the development of pentylenetetrazol (PTZ) kindling and compare its effectiveness with the more commonly used treatment, phenytoin. Kindling was induced in rats by repeated injections (every 24 h) of PTZ (37.5 mg/kg). The rats were subjected to either MFES (0.2 mA in intensity for a 160 ms duration with a 160 ms interval for 20 min) or phenytoin (30 mg/kg) before PTZ injections. Following this treatment, rats received MFES every other day for 10 days or 26 days after establishment of PTZ kindling. The data showed that MFES significantly inhibited development of chemical kindling induced by PTZ in rats (p = 0.001, as compared to PTZ-treated animals). This inhibitory effect is comparable with the effect of 30 mg/kg doses of phenytoin (P = 0.99, as compared to phenytoin group). However, 10 days or 26 days durations of MFES had no effect on established kindled seizures (P = 0.58 as compared to PTZ-treated animals). Our data demonstrate that although MFES significantly inhibited the development of chemical kindling, this experimental paradigm had no effect on established kindled seizures.

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“…In this study, seizure severity consistently increased in rats treated with PTZ, which is in accordance with the results of earlier studies [17,18].…”

Section: Discussionsupporting

confidence: 93%

Mild foot electrical stimulation is comparable with phenytoin in inhibiting pentylenetetrazol-induced kindling in rats

et al. 2019

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“…VEGF alteration in CA1, CA3, and DG in the hippocampus, motor cortex, and cerebellum has been associated with multiple neuropsychiatric diseases, such as cerebral ischemia (Zhou et al., 2017; Song et al., 2019), brain injury (Xu et al., 2016), epilepsy (Choi, Lee, Chang, et al., 2016; Tawfik et al., 2018), and depression (Wang et al., 2014; Seong et al., 2018). Especially, in recent studies on epilepsy, a large body of evidence has emerged suggesting that VEGF not only regulates angiogenesis and vascular permeability but is also involved in neuronal protection in hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Role of NDEL1 and VEGF/VEGFR-2 in Mouse Hippocampus After Status Epilepticus

et al. 2020

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Nuclear-distribution element-like 1 (NDEL1) is associated with the proliferation and migration of neurons. Vascular endothelial growth factor (VEGF) in combination with VEGF receptor-2 (VEGFR-2) regulates the proliferation and migration of neurons. This study was performed to explore undefined alterations in the expression levels of NDEL1 and VEGF/VEGFR-2 within the hippocampus after status epilepticus (SE). Following the creation of pilocarpine-induced epilepsy models using adolescent male C57BL/6 mice, Western blotting and reverse transcription quantitative polymerase chain reaction were applied to assess the levels of NDEL1, VEGF, and VEGFR-2 expression in whole hippocampi at 1, 2, 3, and 4 weeks post-SE, respectively. Immunofluorescent labeling was also employed to detect the colocalization of NDEL1 and VEGF in the hippocampus. Our results indicated that NDEL1 and VEGF have similar patterns of upregulation throughout the hippocampus. Upregulation of VEGFR-2 occurred only in the early stages, and the expression decreased shortly afterward. NDEL1 and VEGF were coexpressed in the cornu ammonis 3 pyramidal cell, granular, and polymorph layers of the dentate gyrus in the hippocampus. This study revealed that NDEL1, VEGF, and VEGFR-2 may work together and are involved in the pathophysiology in the hippocampus after SE.

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“…The authors attributed this reduction to the ability of selenium to down-regulate NOS. 60 Selenium-enriched probiotics were found to inhibit oxidative stress following heat stress through stimulating the activity of antioxidant molecules along with Hsp70. 61 Neuroinflammation is tightly linked with epileptic seizures.…”

Section: Dovepressmentioning

confidence: 99%

<p>Selenium Nanoparticles Pre-Treatment Reverse Behavioral, Oxidative Damage, Neuronal Loss and Neurochemical Alterations in Pentylenetetrazole-Induced Epileptic Seizures in Mice</p>

Yuan¹,

Fu²,

Ji³

et al. 2020

IJN

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Introduction: Epilepsy is a chronic neurological condition characterized by behavioral, molecular, and neurochemical alterations. Current antiepileptic drugs are associated with various adverse impacts. The main goal of the current study is to investigate the possible anticonvulsant effect of selenium nanoparticles (SeNPs) against pentylenetetrazole (PTZ)mediated epileptic seizures in mice hippocampus. Sodium valproate (VPA) was used as a standard anti-epileptic drug. Methods: Mice were assigned into five groups (n=15): control, SeNPs (5 mg/kg, orally), PTZ (60 mg/kg, intraperitoneally), SeNPs+PTZ and VPA (200 mg/kg)+PTZ. All groups were treated for 10 days. Results: PTZ injection triggered a state of oxidative stress in the hippocampal tissue as represented by the elevated lipoperoxidation, heat shock protein 70 level, and nitric oxide formation while decreased glutathione level and antioxidant enzymes activity. Additionally, the blotting analysis showed downregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the epileptic mice. A state of neuroinflammation was recorded following the developed seizures represented by the increased pro-inflammatory cytokines. Moreover, neuronal apoptosis was recorded following the development of epileptic convulsions. At the neurochemical level, acetylcholinesterase activity and monoamines content were decreased in the epileptic mice, accompanied by high glutamate and low GABA levels in the hippocampal tissue. However, SeNP supplementation was found to delay the onset and decreased the duration of tonic, myoclonic, and generalized seizures following PTZ injection. Moreover, SeNPs were found to provide neuroprotection through preventing the development of oxidative challenge via the upregulation of Nrf2 and HO-1, inhibiting the inflammatory response and apoptotic cascade. Additionally, SeNPs reversed the changes in the activity and levels of neuromodulators following the development of epileptic seizures. Conclusion: The obtained results suggest that SeNPs could be used as a promising anticonvulsant drug due to its potent antioxidant, anti-inflammatory, and neuromodulatory activities.

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Neuroprotective mechanisms of sildenafil and selenium in PTZ-kindling model: Implications in epilepsy

Cited by 42 publications

References 77 publications

Mild foot electrical stimulation is comparable with phenytoin in inhibiting pentylenetetrazol-induced kindling in rats

Mild foot electrical stimulation is comparable with phenytoin in inhibiting pentylenetetrazol-induced kindling in rats

Role of NDEL1 and VEGF/VEGFR-2 in Mouse Hippocampus After Status Epilepticus

<p>Selenium Nanoparticles Pre-Treatment Reverse Behavioral, Oxidative Damage, Neuronal Loss and Neurochemical Alterations in Pentylenetetrazole-Induced Epileptic Seizures in Mice</p>

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