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<p>This study investigates the multi-target mechanisms of <i>Atractylodes macrocephala</i> (AM) and its main active component, <i>Atractylenolide III</i> (ATR-III), in mitigating central nervous system (CNS) inflammatory responses in pediatric epilepsy via modulation of the nuclear factor kappa-B (NF-κB) signaling pathway. Network pharmacology identified AM’s active components and their targets, which were integrated with pediatric epilepsy-related targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed potential mechanisms, while molecular docking assessed the binding capacity of ATR-III to key targets. In vitro, an LPS-induced microglial inflammation model was used, with CCK-8 assays, Western blot, qPCR, and JC-1 staining evaluating ATR-III’s effects on cell viability, NF-κB activation, inflammatory cytokine expression, and mitochondrial function. Network pharmacology showed AM’s targets overlap with pediatric epilepsy targets, enriched in neuroinflammation pathways. Molecular docking confirmed ATR-III’s strong binding to NF-κB targets. In vitro, ATR-III significantly suppressed NF-κB activation, reduced p65 and IκBα phosphorylation, decreased inflammatory cytokines, and improved LPS-induced mitochondrial dysfunction by restoring membrane potential and upregulating PGC-1α and COX4. This study elucidates AM and ATR-III’s mechanisms in reducing CNS inflammation and improving mitochondrial function, offering a theoretical basis for AM’s use in pediatric epilepsy and highlighting ATR-III’s potential as a natural anti-inflammatory drug.</p>

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Atractylodes macrocephala compounds attenuate pediatric epilepsy neuroinflammation through multitarget regulation of the NF-κB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月10日

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  • Aiyuan Cai,
  • Ran Liu,
  • Zilong Li,
  • Hailong Huang,
  • Jing Xiao,
  • Yuanhong Lin,
  • Haixia Wu,
  • Ping Liu,
  • Jing Ying,
  • Qingpeng Hu

摘要

This study investigates the multi-target mechanisms of Atractylodes macrocephala (AM) and its main active component, Atractylenolide III (ATR-III), in mitigating central nervous system (CNS) inflammatory responses in pediatric epilepsy via modulation of the nuclear factor kappa-B (NF-κB) signaling pathway. Network pharmacology identified AM’s active components and their targets, which were integrated with pediatric epilepsy-related targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed potential mechanisms, while molecular docking assessed the binding capacity of ATR-III to key targets. In vitro, an LPS-induced microglial inflammation model was used, with CCK-8 assays, Western blot, qPCR, and JC-1 staining evaluating ATR-III’s effects on cell viability, NF-κB activation, inflammatory cytokine expression, and mitochondrial function. Network pharmacology showed AM’s targets overlap with pediatric epilepsy targets, enriched in neuroinflammation pathways. Molecular docking confirmed ATR-III’s strong binding to NF-κB targets. In vitro, ATR-III significantly suppressed NF-κB activation, reduced p65 and IκBα phosphorylation, decreased inflammatory cytokines, and improved LPS-induced mitochondrial dysfunction by restoring membrane potential and upregulating PGC-1α and COX4. This study elucidates AM and ATR-III’s mechanisms in reducing CNS inflammation and improving mitochondrial function, offering a theoretical basis for AM’s use in pediatric epilepsy and highlighting ATR-III’s potential as a natural anti-inflammatory drug.