﻿<?xml version="1.0" encoding="UTF-8"?>
<ArticleSet>
  <Article>
    <Journal>
      <PublisherName>Shahrekord University of Medical Sciences</PublisherName>
      <JournalTitle>Journal of Herbmed Pharmacology</JournalTitle>
      <Issn>2345-5004</Issn>
      <Volume>15</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2026</Year>
        <Month>10</Month>
        <DAY>01</DAY>
      </PubDate>
    </Journal>
    <ArticleTitle>Antiepileptic potential of the aqueous extract of Crassocephalum bauchiense (Hutch.) Milne-Redh. (Asteraceae) in a kainate induced mouse model of temporal lobe epilepsy</ArticleTitle>
    <FirstPage>525</FirstPage>
    <LastPage>537</LastPage>
    <ELocationID EIdType="doi">10.34172/jhp.54007</ELocationID>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Tchang Alkali</FirstName>
        <LastName>Wangbara</LastName>
        <Identifier Source="ORCID">https://orcid.org/0009-0005-7524-9155</Identifier>
      </Author>
      <Author>
        <FirstName>Kidjama Ngo</FirstName>
        <LastName>Ngimout</LastName>
        <Identifier Source="ORCID">https://orcid.org/0009-0007-4491-8912</Identifier>
      </Author>
      <Author>
        <FirstName>Joseph</FirstName>
        <LastName>Ngaibi</LastName>
        <Identifier Source="ORCID">https://orcid.org/0009-0007-1437-300X</Identifier>
      </Author>
      <Author>
        <FirstName>Stephanie Jacqueline Kameni</FirstName>
        <LastName>Njapdounke</LastName>
        <Identifier Source="ORCID">https://orcid.org/0009-0006-4926-0294</Identifier>
      </Author>
      <Author>
        <FirstName>Jean-Jacques Kodji</FirstName>
        <LastName>Midala</LastName>
        <Identifier Source="ORCID">https://orcid.org/0009-0007-5664-8729</Identifier>
      </Author>
      <Author>
        <FirstName>Adrien Tchachoua</FirstName>
        <LastName>Lamare</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0001-8219-4301</Identifier>
      </Author>
      <Author>
        <FirstName>Germain Sotoing</FirstName>
        <LastName>Taiwe</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0002-7771-0268</Identifier>
      </Author>
      <Author>
        <FirstName>Elisabeth Ngo</FirstName>
        <LastName>Bum</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0002-7686-3764</Identifier>
      </Author>
    </AuthorList>
    <PublicationType>Journal Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.34172/jhp.54007</ArticleId>
    </ArticleIdList>
    <History>
      <PubDate PubStatus="received">
        <Year>2026</Year>
        <Month>06</Month>
        <Day>21</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2026</Year>
        <Month>08</Month>
        <Day>16</Day>
      </PubDate>
    </History>
    <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 &lt; 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 &lt; 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 &lt; 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.</Abstract>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Plant extracts</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Temporal lobe epilepsy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Gamma‑aminobutyric acid</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cytokines</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Neuroprotection</Param>
      </Object>
    </ObjectList>
  </Article>
</ArticleSet>