Thymoquinone and Vitamin C Attenuates Pentylenetetrazole-Induced Seizures Via Activation of GABA(B1) Receptor in Adult Rats Cortex and Hippocampus
- Authors
- Ullah, Ikram; Badshah, Haroon; Naseer, Muhammad Imran; Lee, Hae Young; Kim, Myeong Ok
- Issue Date
- Mar-2015
- Publisher
- HUMANA PRESS INC
- Keywords
- Thymoquinone; Pentylenetetrazol; Seizures; Neuroprotection; Antiepileptic; Vitamin C
- Citation
- NEUROMOLECULAR MEDICINE, v.17, no.1, pp.35 - 46
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEUROMOLECULAR MEDICINE
- Volume
- 17
- Number
- 1
- Start Page
- 35
- End Page
- 46
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/17387
- DOI
- 10.1007/s12017-014-8337-3
- ISSN
- 1535-1084
- Abstract
- Epilepsy is a common neurological disorder that leads to neuronal excitability and provoke various forms of cellular reorganization in the brain. In this study, we investigate the anti-convulsant and neuroprotective effects of thymoquinone (TQ) and vitamin C against pentylenetetrazole (PTZ)-induced generalized seizures. Epileptic seizures were induced in adult rats using systemic intraperitoneal injections of PTZ (50 mg/kg) for 7 days. Animals pretreated with either TQ or vitamin C or in combination attenuated PTZ-induced seizures and mortality in rats as well neurodegeneration in the cells. Compared to PTZ, TQ and vitamin C significantly prolonged the onset of seizures (p > 0.05) as well decrease the high-grade seizures. Analysis of electroencephalogram (EEG) recordings revealed that TQ or vitamin C supplementation significantly reduced polyspike and epileptiform discharges. Epileptic seizures caused a decline in expression of gamma-aminobutyric acid B1 receptor (GABA(B1)R) (p > 0.05), unchanged expression of protein kinase A (PKA), decreased calcium/calmodulin-dependent protein kinase II (CaMKII) (p > 0.05) and inhibit the phosphorylation of cAMP response element-binding protein (CREB) (p > 0.05) in cortex and hippocampus, respectively, compared with control. Changes in expression of GABA(B1)R, CaMKII and CREB by PTZ were reversed by TQ and vitamin C supplementation. Moreover, PTZ significantly increased Bax, decreased Bcl-2 expression and finally the activation of caspase-3. TQ and vitamin C pretreatment reversed all these deleterious effects induced by PTZ. TQ and vitamin C showed anticonvulsant effects via activation of GABA(B1)R/CaMKII/CREB pathway and suggest a potential therapeutic role in epilepsy.
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