Abstract
Introduction: Temporal lobe epilepsy (TLE) is characterized by an imbalance between excitatory and inhibitory systems associated with neuroinflammation. These mechanisms contribute to therapeutic resistance and disease progression. Crassocephalum bauchiense (Hutch.) Milne-Redh. (Asteraceae) has traditionally been used in the management of convulsions and epilepsy. This study aimed to investigate the antiepileptic potential of C. bauchiense in a kainate‑induced mouse model of TLE.
Methods: In this experimental study, a single intraperitoneal injection of kainate (15 mg/kg) was used to induce status epilepticus (SE). Over the following two weeks, mice received daily oral treatment with distilled water, sodium valproate (300 mg/kg), or C. bauchiense extract (280, 140, 70, and 28 mg/kg). Seizure susceptibility was tested with pentylenetetrazol (15 mg/kg, i.p.), and hippocampal gamma‑aminobutyric acid (GABA), GABA aminotransferase (GABA‑T), and cytokines were measured.
Results: The extract increased (P < 0.001) seizure latency by 58.9-175% (doses 70-280 mg/kg), reduced duration and frequency of recurrent seizures, and at 140-280 mg/kg showed effects comparable to sodium valproate. GABA rose by 49.32%, while GABA‑T decreased by 57.64% at the highest dose, restoring inhibitory neurotransmission (P < 0.001). Interleukin 1 beta (IL‑1β), interleukin 6 (IL‑6), interferon gamma (IFN‑γ) and tumor necrosis factor alpha (TNF‑α) were suppressed in a dose-dependent fashion, with the strongest effects (P < 0.001) observed at the higher doses. Moreover, the dysregulated level of interleukin‑10 (IL‑10) was corrected by the treatment.
Conclusion: The antiepileptic effects were associated with restoration of GABAergic signaling and attenuation of neuroinflammatory markers. These results support the future development of C. bauchiense as a source of bioactive compounds with antiepileptic potential.