P.476 Treatment with topiramate and lacosamide during status epilepticus attenuates motor seizure and oxidative stress in rats

2020 ◽  
Vol 40 ◽  
pp. S269-S270
Author(s):  
M. Shishmanova-Doseva ◽  
J. Tchekalarova ◽  
L. Ioanidu ◽  
Y. Uzunova ◽  
M. Atanasova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Motor Seizure ◽  
And Oxidative Stress

scholarly journals Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish

2021 ◽  
Author(s):  
Ana Caroline Salvador de Farias ◽  
Karolyne de Pieri Pickler ◽  
Henrique Teza Bernardo ◽  
Samira Leila Baldin ◽  
Eduardo Ronconi Dondossola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Kainic Acid ◽  
Glutamate Transport ◽  
And Oxidative Stress

scholarly journals Melatonin Pretreatment Protects Against Status Epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish

2021 ◽  
Author(s):  
Ana Caroline Salvador de Farias ◽  
Karolyne de Pieri Pickler ◽  
Henrique Teza Bernardo ◽  
Samira Leila Baldin ◽  
Eduardo Ronconi Dondossola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Kainic Acid ◽  
Neuronal Damage ◽  
Glutamate Uptake ◽  
Radical Scavenging ◽  
Antioxidant Enzyme Activities ◽  
Melatonin Treatment ◽  
Zebrafish Brain ◽  
And Oxidative Stress

Abstract Status epilepticus (SE) develops from abnormal electrical discharges, resulting in neuronal damage. Current treatments include antiepileptic drugs. However, the most common drugs used to treat seizures may sometimes be ineffective and have many side effects. Melatonin is an endogenous physiological hormone that is considered an alternative treatment for neurological disorders because of its free radical scavenging property. Thus, this study aimed to determine the effects of melatonin pretreatment on SE by inducing glutamatergic hyperstimulation in zebrafish. Seizures were induced in zebrafish using kainic acid (KA), a glutamate analog, and the seizure intensity was recorded for 60 min. Melatonin treatment for 7 days showed a decrease in seizure intensity (28%), latency to reach score 5 (14 min), and duration of SE (29%). In addition, melatonin treatment attenuated glutamate transporter levels, which significantly decreased in the zebrafish brain after 12 h of KA-induced seizures. Melatonin treatment reduced the increase in oxidative stress by reactive oxygen species formation through thiobarbituric acid reactive substances and 2‘,7‘-dichiorofluorescin, induced by KA-seizure. An imbalance of antioxidant enzyme activities such as superoxide dismutase and catalase was influenced by melatonin and KA-induced seizures. Our study indicates that melatonin promotes a neuroprotective response against the epileptic profile in zebrafish. These effects could be related to the modulation of glutamatergic neurotransmission, recovery of glutamate uptake, and oxidative stress parameters in the zebrafish brain.

scholarly journals Effect of naringenin (A naturally occurring flavanone) against pilocarpine-induced status epilepticus and oxidative stress in mice

2017 ◽  
Vol 13 (49) ◽  
pp. 154 ◽  
Author(s):  
Nahida Tabassum ◽  
Sheeba Shakeel ◽  
MuneebU Rehman ◽  
Umar Amin ◽  
Manzoorur Rahman Mir
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Naturally Occurring ◽  
And Oxidative Stress

scholarly journals The Effects of Quinacrine, Proglumide, and Pentoxifylline on Seizure Activity, Cognitive Deficit, and Oxidative Stress in Rat Lithium-Pilocarpine Model of Status Epilepticus

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Mohammad Ahmad ◽  
Gasem M. Abu-Taweel ◽  
Ahmad E. Aboshaiqah ◽  
Jamaan S. Ajarem
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Glutathione S Transferase ◽  
Adult Rats ◽  
Cognitive Dysfunctions ◽  
Mature Brain ◽  
Pilocarpine Model ◽  
And Oxidative Stress

The present data indicate that status epilepticus (SE) induced in adult rats is associated with cognitive dysfunctions and cerebral oxidative stress (OS). This has been demonstrated using lithium-pilocarpine (Li-Pc) model of SE. OS occurring in hippocampus and striatum of mature brain following SE is apparently due to both the increased free radicals production and the limited antioxidant defense. Pronounced alterations were noticed in the enzymatic, glutathione-S transferase (GST), catalase (CAT), and superoxide dismutase (SOD), as well as in the nonenzymatic; thiobarbituric acid (TBARS) and reduced glutathione (GST), indices of OS in the hippocampus and striatum of SE induced animals. Quinacrine (Qcn), proglumide (Pgm), and pentoxifylline (Ptx) administered to animals before inducing SE, were significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral OS. The findings suggest that all the drugs were effective in the order of Ptx < Pgm < Qcn indicating that these drugs are potentially antiepileptic as well as antioxidant; however, further studies are needed to establish this fact. It can be assumed that these antiepileptic substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment of epilepsy through ameliorating the cerebral OS.

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