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<p>Dehydroeffusol, a unique <i>Juncus effusus</i> phenanthrene, ameliorates neurodegeneration in the dentate granule cell layer, which is most vulnerable to amyloid β<sub>1-42</sub> (Aβ<sub>1-42</sub>) neurotoxicity in the hippocampus. We tested the ameliorating effect of effusol, another unique <i>Juncus effusus</i> phenanthrene. Effusol (15 mg/kg) was orally delivered to mice once a day for 2 days, and mice were subjected to intracerebroventricular (ICV) administration of Aβ<sub>1-42</sub> 1 day after the last deliver of effusol according to published protocol in the analysis of dehydroeffusol. Fourteen days later, effusol ameliorated neurotoxicity in the dentate granule cell layer evaluated by propidium iodide. Effusol did not increase the synthesis of metallothioneins (MTs) for capturing toxic Zn<sup>2+</sup> ferried by Aβ<sub>1-42</sub>, unlike the effect of dehydroeffusol via MT synthesis. However, effusol reduced both intracellular increases in Zn<sup>2+</sup> and reactive oxygen species (ROS) by Aβ<sub>1-42</sub>. To test the effect of post-intake of effusol, mice were subjected to ICV administration of Aβ<sub>1-42</sub>, and effusol was delivered to mice in the same manner. Effusol ameliorated Aβ<sub>1-42</sub>-mediated neurotoxicity. These results first suggest that effusol ameliorates Aβ<sub>1-42</sub>-mediated neurotoxicity in the dentate gyrus by reducing intracellular ROS generation, which is induced by Zn<sup>2+</sup> dysregulation. It is likely that oral intake of effusol may protectively act on Aβ<sub>1-42</sub> neurotoxicity. The evidence that effusol ameliorates Zn<sup>2+</sup> dysregulation as a trigger in the Aβ<sub>1-42</sub> pathogenesis may contribute to developing a preventive nutrient against the Aβ<sub>1-42</sub> pathogenesis.</p>

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Effusol, a unique Juncus effusus phenanthrene, ameliorates amyloid β1-42-mediated neurotoxicity in mice

  • 期刊论文

  • 发表日期：

    2025年7月17日

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  • Haruna Tamano,
  • Daichi Murakami,
  • Toshiyuki Fukuda,
  • Yasuhito Akagi,
  • Shinji Ikeura,
  • Atsushi Takeda

摘要

Dehydroeffusol, a unique Juncus effusus phenanthrene, ameliorates neurodegeneration in the dentate granule cell layer, which is most vulnerable to amyloid β1-42 (Aβ1-42) neurotoxicity in the hippocampus. We tested the ameliorating effect of effusol, another unique Juncus effusus phenanthrene. Effusol (15 mg/kg) was orally delivered to mice once a day for 2 days, and mice were subjected to intracerebroventricular (ICV) administration of Aβ1-42 1 day after the last deliver of effusol according to published protocol in the analysis of dehydroeffusol. Fourteen days later, effusol ameliorated neurotoxicity in the dentate granule cell layer evaluated by propidium iodide. Effusol did not increase the synthesis of metallothioneins (MTs) for capturing toxic Zn2+ ferried by Aβ1-42, unlike the effect of dehydroeffusol via MT synthesis. However, effusol reduced both intracellular increases in Zn2+ and reactive oxygen species (ROS) by Aβ1-42. To test the effect of post-intake of effusol, mice were subjected to ICV administration of Aβ1-42, and effusol was delivered to mice in the same manner. Effusol ameliorated Aβ1-42-mediated neurotoxicity. These results first suggest that effusol ameliorates Aβ1-42-mediated neurotoxicity in the dentate gyrus by reducing intracellular ROS generation, which is induced by Zn2+ dysregulation. It is likely that oral intake of effusol may protectively act on Aβ1-42 neurotoxicity. The evidence that effusol ameliorates Zn2+ dysregulation as a trigger in the Aβ1-42 pathogenesis may contribute to developing a preventive nutrient against the Aβ1-42 pathogenesis.