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Abstract <p>Neuroinflammatory processes and oxidative imbalance are key contributors to the onset and development of seizures. Betahistine, a structural analog of histamine, has recently gained attention for its anticonvulsant, antiepileptic, and neuroprotective effects. However, its impact on inflammatory and oxidative stress (OS) markers in epileptic seizures has not yet been clarified. This research aimed to evaluate the effect of betahistine on seizure activity, OS, and inflammation markers in a pentylenetetrazole (PTZ)-induced seizure model. Twenty-eight Wistar albino rats were randomly assigned to one control group and three experimental groups. Animals in the test groups were administered betahistine at doses of 1 or 10 mg/kg or saline (1 mL/kg) for a continuous period of eight days. On the eighth day, 30 minutes after the final treatment, a single i.p. injection of PTZ (65 mg/kg) was administered to induce acute seizures. Seizure latencies, including first myoclonic jerk-(FMJ), tonic generalized extension-(TGE), and generalized clonic seizures-(GCS), were recorded for 30 min. Brain OS and proinflammatory cytokine levels were assessed using ELISA. No significant differences in seizure latencies were observed among the groups. PTZ administration significantly reduced SOD and GSH-Px levels, while increasing IL-1β levels (<i>p</i> &lt; 0.05). Administration of 1 mg/kg betahistine significantly decreased levels of TNF-α, IL-1β, and IL-6 when compared to the PTZ + S group. Additionally, at the 10 mg/kg dose, a reduction in IL-1β levels was also observed compared to the PTZ + S group (<i>p</i> &lt; 0.05). These findings suggest that betahistine at 1 mg/kg improves antioxidant defenses while attenuating inflammatory cytokine levels in a PTZ-induced acute seizure model.</p>

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Investigation of Antiepileptic, Anti-Inflammatory and Antioxidative Potential of Betahistine in a Pentylenetetrazole-Induced Acute Seizure Model

  • 期刊论文

  • 发表日期：

    2026年3月1日

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  • Ozlem Turgut,
  • Ozlem Ergul,
  • Zubeyir Huyut,
  • Bunyamin Ucar

摘要

Abstract

Neuroinflammatory processes and oxidative imbalance are key contributors to the onset and development of seizures. Betahistine, a structural analog of histamine, has recently gained attention for its anticonvulsant, antiepileptic, and neuroprotective effects. However, its impact on inflammatory and oxidative stress (OS) markers in epileptic seizures has not yet been clarified. This research aimed to evaluate the effect of betahistine on seizure activity, OS, and inflammation markers in a pentylenetetrazole (PTZ)-induced seizure model. Twenty-eight Wistar albino rats were randomly assigned to one control group and three experimental groups. Animals in the test groups were administered betahistine at doses of 1 or 10 mg/kg or saline (1 mL/kg) for a continuous period of eight days. On the eighth day, 30 minutes after the final treatment, a single i.p. injection of PTZ (65 mg/kg) was administered to induce acute seizures. Seizure latencies, including first myoclonic jerk-(FMJ), tonic generalized extension-(TGE), and generalized clonic seizures-(GCS), were recorded for 30 min. Brain OS and proinflammatory cytokine levels were assessed using ELISA. No significant differences in seizure latencies were observed among the groups. PTZ administration significantly reduced SOD and GSH-Px levels, while increasing IL-1β levels (p < 0.05). Administration of 1 mg/kg betahistine significantly decreased levels of TNF-α, IL-1β, and IL-6 when compared to the PTZ + S group. Additionally, at the 10 mg/kg dose, a reduction in IL-1β levels was also observed compared to the PTZ + S group (p < 0.05). These findings suggest that betahistine at 1 mg/kg improves antioxidant defenses while attenuating inflammatory cytokine levels in a PTZ-induced acute seizure model.