• Emorfazone Attenuates NF-κB Gene Expression in a PTZ-Induced Seizure Model in Male Wistar Rats
  • Fatemeh Mirjalili,1 Arian khajehzadeh dezfouli,2 Mehdi Khezri,3 Fatemeh Fayaz sarcheshmeh,4 Haniyeh verdizadeh,5 Abdolkarim Hosseini,6,*
    1. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University
    2. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University
    3. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University
    4. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University
    5. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University
    6. Faculty of Life Sciences and Biotechnology, Shahid Beheshti University


  • Introduction: Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures due to abnormal electrical discharges in the brain. Although numerous antiepileptic drugs are available, treatment resistance remains a significant challenge, especially in patients with refractory epilepsy. Recent studies highlight the role of neuroinflammation in epilepsy pathogenesis, with the nuclear factor-kappa B (NF-κB) signaling pathway being a key mediator of seizure-induced inflammatory processes. Emorfazone, a nonsteroidal anti-inflammatory drug (NSAID), has shown potential neuroprotective properties in preclinical models. This study aims to evaluate the anti-inflammatory and neuroprotective effects of Emorfazone in a PTZ-induced seizure model in rats, focusing on modulation of the NF-κB pathway
  • Methods: Twenty male Wistar rats were randomly assigned to four groups (n=5 per group): Group 1: Healthy control (saline only) Group 2: PTZ control (PTZ only) Groups 3 & 4: Emorfazone-treated (0.6 mg/kg and 1.2 mg/kg, i.p.) Thirty minutes after Emorfazone or saline injection, PTZ was administered (except to Group 1). Following seizure induction, animals were euthanized and brains collected. NF-κB gene expression was quantified using qRT-PCR.
  • Results: PTZ administration significantly increased NF-κB gene expression compared to healthy controls, confirming a strong neuroinflammatory response. Pre-treatment with Emorfazone attenuated this upregulation in a statistically significant manner at both tested doses, suggesting a dose-responsive anti-inflammatory effect.
  • Conclusion: Emorfazone demonstrated a significant anti-inflammatory effect by reducing NF-κB gene expression in the brains of PTZ-induced epileptic rats. These findings indicate its potential neuroprotective role in seizure-related neuroinflammation.
  • Keywords: Epilepsy/NF-κB signaling pathway/Emorfazone/Neuroinflammation/PTZ-induced seizure model