The Effect of Valproic Acid on DNA Damage and Apoptosis After Pentylenetetrazole-induced Epileptic Seizure Generated in the Hippocampus and Cortex in Rats

Ekici, Mahmut; Taşkıran, Ahmet Şevki

doi:10.21597/jist.730381

Cited by 2 publications

(2 citation statements)

References 19 publications

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“…The function of the antioxidant effect in the treatment of antiepileptic drugs is controversial. The experimental study conducted by Ekici et al reported the effect of valproic acid pre-treatment, an anti-epileptic drug, on increasing DNA damage before epileptic seizures (Ekici and Taşkiran, 2020). In their study, Filiz and Öztürk showed that pre-treatment with carbamazepine enhanced TOS and MDA levels in glutamate-derived cells (Filiz and Öztürk, 2021).…”

Section: Resultsmentioning

confidence: 99%

Levetiracetam Protects Against Glutamate-Induced Excitotoxicity in SH-SY5Y Cell Line

ÇİLTAŞ

GÜNDOĞDU

Yulak

2022

International Journal of Nature and Life Sciences

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The latest research has shown that the new generation of antiepileptic drugs has neuroprotective on nervous system. On the other hand, the effect of levetiracetam, a new generation antiepileptic drug, on GIC in SH-SY5Y cells remains uncertain. This research aims to investigate the effect of levetiracetam on GIC and oxidant and antioxidant levels in SH-SY5Y cells. It is utilized SH-SY5Y cell line at this research. Four groups were formed to assess the impact of levetiracetam on SH-SY5Y cell death following GIC. While no treatment was administered to the control group, 10 mM glutamate was administered to the glutamate group for 24 hours (10, 25, 50 and 100 μg/ml). LEV at different concentrations was given to the levetiracetam for 24 hours. The levetiracetam + glutamate was pretreated with levetiracetam at several concentrations for 1 hour (10, 25, 50, and 100 μg/ml), which was followed by a 24-hour exposure to 10 mM glutamate. TAS and TOS levels in cells and cell viability were examined. Following the GIC, a 25 μg/ml-Levetiracetam improved cell viability in neuroblastoma cells dramatically (p < 0.05). LEV (25 ug/ml) + glutamate while enhanced TAS levels in neuroblastoma cells in comparison to the glutamate (p < 0.05), significantly reduced TOS levels (p < 0.05 Levetiracetam improves cell survival by reducing cell death following GIC in neuroblastoma cells. In the acute process, levetiracetam exerts a protective effect.

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Section: Resultsmentioning

confidence: 99%

Levetiracetam Protects Against Glutamate-Induced Excitotoxicity in SH-SY5Y Cell Line

ÇİLTAŞ

GÜNDOĞDU

Yulak

2022

International Journal of Nature and Life Sciences

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“…The relationship between membrane lipid peroxidation, neuronal excitotoxicity, antioxidants, and AEDs was reviewed by Hamed and Abdellah (SA & MM, 2004). Ekici et al, in their experimental study, showed that valproic acid pretreatment, which is an AED before epileptic seizures, has a DNA damage-increasing effect(EKİCİ & TAŞKIRAN, 2020). Oxidative damage induced by CBZ was demostrated by some previously conducted researches (C. M…”

mentioning

confidence: 98%

The Effect of Carbamazepine Against Glutamate-induced Cytotoxicity in the C6 Cell Line

Filiz¹,

Öztürk²

2021

JSTR

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Recent studies have shown that carbamazepine has positive effects on nervous system. However, its effect on glutamate-induced cytotoxicity in glial cells is still unclear. Our study was designed to investigate the effect of carbamazepine against glutamate-induced cytotoxicity in C6 glial cells and involved mechanisms. Material and Methods:In this study, the C6 glioma cell line was used. Four cell groups were prepared to evaluate the effect of carbamazepine on glial cell death after glutamate-induced cytotoxicity. The control group was without any treatment. Cells in the glutamate group were treated with 10 mM glutamate for 24 hours. Cells in the carbamazepine group were treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 24 hours. Cells in the carbamazepine + glutamate group were pre-treated with various concentrations (3.75, 7.5, 15, and 30 μM) of carbamazepine for 1 hour and then exposed to 10 mM glutamte for 24 hours. The cell viability was evaluated by XTT assay. Total antioxidant status (TAS), total oxidant status (TOS), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA) levels in the cells were measured by commercial kits.Results: Carbamazepine at the concentration of 30 μM significantly increased the cell viability in C6 cells after glutamate-induce cytotoxicity (p < 0.05). CBZ (30 µM) + glutamate significantly increased TOS levels in C6 cells compared to control untreated control cells (p < 0.05), while it did not change TAS level (p > 0.05). Moreover, carbamazepine did not change TNF-α level (p > 0.05) and increased MDA (p< 0.05) level in C6 cells after glutamate-induced cytotoxicity. Conclusion:Carbamazepine decreases glial cell death after glutamate-induced cytotoxicity in C6 cells. While carbamazepine produced protective effective in the acute process, long-term usage may increase oxidative damage and cause cell death.

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The Effect of Valproic Acid on DNA Damage and Apoptosis After Pentylenetetrazole-induced Epileptic Seizure Generated in the Hippocampus and Cortex in Rats

Cited by 2 publications

References 19 publications

Levetiracetam Protects Against Glutamate-Induced Excitotoxicity in SH-SY5Y Cell Line

Levetiracetam Protects Against Glutamate-Induced Excitotoxicity in SH-SY5Y Cell Line

The Effect of Carbamazepine Against Glutamate-induced Cytotoxicity in the C6 Cell Line

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