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Year : 2018  |  Volume : 14  |  Issue : 59  |  Page : 520-527

Elucidation of the molecular mechanism of tempol in pentylenetetrazol-induced epilepsy in mice: Role of gamma-aminobutyric acid, tumor necrosis factor-alpha, interleukin-1β and c-Fos

1 Department of Internal Neurology, Cangzhou Central Hospital, Cangzhou, Hebei, China
2 Department of Neurosurgery, Linyi Central Hospital, Linyi, Shandong, China
3 Department of Pharmacology, Poona College of Pharmacy, Bharati Vidyapeeth Deemed University, Pune, Maharashtra, India
4 Innoscience Research SDB BDH, Subang Jaya, Selangor, Malaysia

Correspondence Address:
Subhash L Bodhankar
Department of Pharmacology, Poona College of Pharmacy, Bharati Vidyapeeth Deemed University, Erandwane, Paud Road, Pune - 411 038, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_263_18

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Background: Epilepsy is a chronic neurological disorder occurred due to periodic neuronal discharge and imbalance in brain electrical activity. 4-Hydroxy-TEMPO (Tempol) is a membrane-permeable radical scavenger moiety. Aim: The aim of this study is to evaluate the anticonvulsant potential of tempol against pentylenetetrazol (PTZ)-induced seizures in mice. Materials and Methods: Convulsion was produced in the male Swiss albino mice by administration of PTZ (90 mg/kg, i.p.). Mice were pretreated with either vehicle, tempol (50, 100 and 200 mg/kg, i.p.) or diazepam (5 mg/kg). Various behavioral, biochemical, molecular, and histological parameters were evaluated. Results: Mice pretreated with tempol (100 and 200 mg/kg) showed significantly (P < 0.01 and P < 0.001) delayed-onset on tonic-clonic convulsion, decrease the duration of convulsions and mortality in mice. Intraperitoneal administration of PTZ resulted in significant increase in oxido-nitrosative stress, whereas it significantly (P < 0.01 and P < 0.001) inhibited by the tempol administration. There was significant increased (P < 0.01 and P < 0.001) in the levels of brain monoamines (gamma-aminobutyric acid [GABA] and dopamine) and Na+ K+ ATPase activity, whereas significant decreased (P < 0.01 and P < 0.001) in xanthine oxidase activity in tempol pretreated mice. PTZ-induced up-regulated mRNA expressions of tumor necrosis factor-alpha, interleukin-1 beta , and c-Fos were significantly inhibited (P < 0.01 and P < 0.001) by tempol. It is also significantly down-regulated (P < 0.05 and P < 0.001) immunohistochemical c-Fos expressions. Conclusion: Pretreatment with tempol attenuates PTZ-induced tonic-clonic seizures via its anti-inflammatory, anti-oxidant and GABAergic potential. Abbreviations used: GABA: Gamma-aminobutyric acid; PTZ: Pentylenetetrazol; TNF-α: Tumor necrosis factor-alpha; 4-HT: 4-Hydroxy-TEMPO; DZP: Diazepam; GSH: Reduced glutathione; NO: Nitric oxide; MDA: Malondialdehyde; SOD: Superoxide dismutase; ROS: Reactive oxygen species; IL-1β: Interleukin-1 beta.

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