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<p>Cerebral stroke is characterized by high rate of disability and mortality. Emerging evidence indicates a relationship between acute ischemic stroke and alterations in the intestinal microbiota. Herein, the mechanism of <i>Eucommia ulmoides</i> extract (EUE) within ischemic stroke will be investigated from the perspective of intestinal microflora. In the study, EUE significantly reduced the area of cerebral infarction, ameliorated neurological deficits, and reduced neuronal death in mice. EUE reversed intestinal microbiota deregulation by regulating bacterial abundance, including up-regulating the abundance of the beneficial bacteria <i>Dubosiella</i>, <i>Lachnospiraceae_NK4A136_group</i>, and down-regulating the abundance of the deleterious bacteria <i>Helicobacter</i>, <i>Bifidobacterium</i>, <i>Allobaculum</i>, and <i>Ileibacterium</i> abundance. In addition, EUE also upregulated metabolites associated with inflammation and neuroprotection, including LysoPE, octadecyl fumarate, and adrenic acid. In in vitro experiments, the combination of EUE and LysoPE (0:0/20:4) significantly inhibited apoptosis, inflammatory responses, and oxidative stress levels in OGD cells compared to use alone. In conclusion, EUE significantly alleviated symptoms and neurological deficits in MCAO mice, and its mechanism is related to its involvement in remodeling intestinal microbiota and metabolism. EUE and LysoPE (0:0/20:4) are expected to be a potential novel regimen for the clinical treatment of cerebral ischemic stroke.</p>

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Eucommia ulmoides Oliver (Duzhong) extract ameliorates cerebral ischemic stroke in mice by remodeling intestinal microbiota and metabolites

  • 期刊论文

  • 发表日期：

    2025年11月25日

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  • Xin Qi,
  • Mengyuan Deng,
  • Minhong Li,
  • Wenjia Ma,
  • Yangbo Zhou

摘要

Cerebral stroke is characterized by high rate of disability and mortality. Emerging evidence indicates a relationship between acute ischemic stroke and alterations in the intestinal microbiota. Herein, the mechanism of Eucommia ulmoides extract (EUE) within ischemic stroke will be investigated from the perspective of intestinal microflora. In the study, EUE significantly reduced the area of cerebral infarction, ameliorated neurological deficits, and reduced neuronal death in mice. EUE reversed intestinal microbiota deregulation by regulating bacterial abundance, including up-regulating the abundance of the beneficial bacteria Dubosiella, Lachnospiraceae_NK4A136_group, and down-regulating the abundance of the deleterious bacteria Helicobacter, Bifidobacterium, Allobaculum, and Ileibacterium abundance. In addition, EUE also upregulated metabolites associated with inflammation and neuroprotection, including LysoPE, octadecyl fumarate, and adrenic acid. In in vitro experiments, the combination of EUE and LysoPE (0:0/20:4) significantly inhibited apoptosis, inflammatory responses, and oxidative stress levels in OGD cells compared to use alone. In conclusion, EUE significantly alleviated symptoms and neurological deficits in MCAO mice, and its mechanism is related to its involvement in remodeling intestinal microbiota and metabolism. EUE and LysoPE (0:0/20:4) are expected to be a potential novel regimen for the clinical treatment of cerebral ischemic stroke.