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<p>Parkinson’s disease (PD) involves degeneration of dopaminergic neurons in the substantia nigra (SN) and is closely linked to neuroinflammation. Recent research has shown that PD may originate in the gut, where microbial dysbiosis aggravates disease progression. Evodiamine (EVO), the main active component of <i>Evodia rutaecarpa</i>, has been proven to be effective against various diseases; however, its effects on PD remains unclear. We established 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model to evaluate EVO and elucidate its mechanisms, and found that EVO alleviated motor deficits by suppressing activated microglia and astrocytes, thereby reducing dopaminergic neuronal loss in the SN. EVO treatment decreased the abundance of pro-inflammatory genus <i>Akkermansia</i> and increased the abundance of the anti-inflammatory genera <i>Butyricicoccus</i>, <i>Oscillospira</i>, <i>Ruminococcus</i>, and <i>Coprococcus</i>, thereby inhibiting gut inflammation. It lowered serum levels of interleukin (IL)-6, tumor necrosis factor-α, and IL-1β and upregulated ZO-1 and occludin, preserving the gut and blood–brain barrier integrity. This study implicates toll-like receptor 4 (TLR4)/myeloid differentiation primary response (MyD88)/nuclear factor kappa B (NF-kB) pathway in the inflammatory response, suggesting that EVO exerts neuroprotective effects in PD mice by modulating gut microbiota and suppressing this pathway to inhibit inflammation.</p>

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Evodiamine alleviates MPTP-induced Parkinson’s disease in mice by regulating gut microbiota and suppressing TLR4/MyD88/NF-kB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月13日

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  • Shuo Wang,
  • Yunbo Zhu,
  • Jiuxue Wang,
  • Wei Jin,
  • Na Li,
  • Zhe Li,
  • Yajun Chang,
  • Chao Jiang,
  • Tianjun Wang

摘要

Parkinson’s disease (PD) involves degeneration of dopaminergic neurons in the substantia nigra (SN) and is closely linked to neuroinflammation. Recent research has shown that PD may originate in the gut, where microbial dysbiosis aggravates disease progression. Evodiamine (EVO), the main active component of Evodia rutaecarpa, has been proven to be effective against various diseases; however, its effects on PD remains unclear. We established 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model to evaluate EVO and elucidate its mechanisms, and found that EVO alleviated motor deficits by suppressing activated microglia and astrocytes, thereby reducing dopaminergic neuronal loss in the SN. EVO treatment decreased the abundance of pro-inflammatory genus Akkermansia and increased the abundance of the anti-inflammatory genera Butyricicoccus, Oscillospira, Ruminococcus, and Coprococcus, thereby inhibiting gut inflammation. It lowered serum levels of interleukin (IL)-6, tumor necrosis factor-α, and IL-1β and upregulated ZO-1 and occludin, preserving the gut and blood–brain barrier integrity. This study implicates toll-like receptor 4 (TLR4)/myeloid differentiation primary response (MyD88)/nuclear factor kappa B (NF-kB) pathway in the inflammatory response, suggesting that EVO exerts neuroprotective effects in PD mice by modulating gut microbiota and suppressing this pathway to inhibit inflammation.