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<p>Baicalein, a naturally occurring flavonoid with well-documented anti-inflammatory and neuroprotective effects, has shown therapeutic promise in multiple models of neurological disorders. However, whether baicalein can counteract diquat-induced neurotoxicity remains uncertain. This study reveals that baicalein alleviates diquat-induced neuroinflammation and microglial pyroptosis in mice in a gut microbiota (GM)-dependent manner. In the <i>in vivo</i> experiments, multi-omics analyses demonstrated that baicalein elevates the GM-derived metabolite indole-3-propionic acid (IPA), which was sufficient to suppress pyroptosis. In parallel, IPA was identified as a critical mediator of baicalein's neuroprotective effects, as exogenous IPA administration recapitulated baicalein's protection, and baicalein treatment significantly elevated IPA levels. Mechanistically, through inhibiting the DEAD-box helicase 3 X-linked / GTPase-activating protein (SH3 domain) binding protein 1 pathway by <i>in vitro</i> experiments. Our study demonstrated that baicalein mitigates diquat-induced neuroinflammation, underscoring the therapeutic potential of targeting the GM to counteract herbicide-related neurotoxicity.</p> Graphical Abstract <p></p>

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Pre-treatment with baicalein alleviates the diquat-induced microglial pyroptosis through gut microbiota–derived indole-3-propionic acid and DDX3X/G3BP1 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月10日

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  • Ting Li,
  • Mengxiao Feng,
  • Ping Wang,
  • Miao Jiang,
  • Jaiyu Cui,
  • Mengxia Jin,
  • Congying Song,
  • Liying Lin,
  • Yuan-Qiang Lu

摘要

Baicalein, a naturally occurring flavonoid with well-documented anti-inflammatory and neuroprotective effects, has shown therapeutic promise in multiple models of neurological disorders. However, whether baicalein can counteract diquat-induced neurotoxicity remains uncertain. This study reveals that baicalein alleviates diquat-induced neuroinflammation and microglial pyroptosis in mice in a gut microbiota (GM)-dependent manner. In the in vivo experiments, multi-omics analyses demonstrated that baicalein elevates the GM-derived metabolite indole-3-propionic acid (IPA), which was sufficient to suppress pyroptosis. In parallel, IPA was identified as a critical mediator of baicalein's neuroprotective effects, as exogenous IPA administration recapitulated baicalein's protection, and baicalein treatment significantly elevated IPA levels. Mechanistically, through inhibiting the DEAD-box helicase 3 X-linked / GTPase-activating protein (SH3 domain) binding protein 1 pathway by in vitro experiments. Our study demonstrated that baicalein mitigates diquat-induced neuroinflammation, underscoring the therapeutic potential of targeting the GM to counteract herbicide-related neurotoxicity.

Graphical Abstract