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    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

    Leguo Zhang1, Tao Wu2, Amit Kandhare3, Anwesha Mukherjee3, Gang Guo4, Subhash L. Bodhankar3★★ Corresponding author

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

    CORRESPONDENCE

    Subhash L. Bodhankar

    Department of Pharmacology, Poona College of Pharmacy, Bharati Vidyapeeth Deemed University, Pune, Maharashtra, India.

    drslbodh@gmail.com

    Received: 14-05-2018; Revised: 28-06-2018.

    Volume 14, Issue 59s · pp. S520–S527 · PUBLISHED 17 January 2019 · DOI: 10.4103/pm.pm_263_18

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    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.

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      Zhang, L., Wu, T., Kandhare, A., Mukherjee, A., Guo, G., & Bodhankar, S. L. (2019). 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. Pharmacognosy Magazine, 14(59s), S520–S527. https://doi.org/10.4103/pm.pm_263_18