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<p>Zearalenone (ZEN) is a stable, highly toxic compound that can cause multi-organ toxicity with prolonged exposure. Previous studies have demonstrated that ZEN can damage the physical barrier of the intestinal tract in animals. However, the relationship between ZEN-induced damage to the physical barrier of the intestinal tract in animals, oxidative stress, and the intestinal microbiota remains unclear. Astilbin (ASB) is a natural flavonoid renowned for its potent anti-inflammatory and antioxidant properties. However, whether ASB can alleviate ZEN-induced intestinal damage in mice remains unknown. In this study, we aimed to investigate whether ASB can alleviate ZEN-induced damage to the physical barrier and dysbiosis of the intestinal microbiota in mice. The study selected 36 male BALB/c mice aged 6 weeks, which were randomly divided into the CON group, the ZEN group (ZEN 40&#xa0;mg/kg), the ASB group (ASB 100&#xa0;mg/kg), the L ASB/ZEN group (ASB 25&#xa0;mg/kg + ZEN 40&#xa0;mg/kg), M ASB/ZEN group (ASB 50&#xa0;mg/kg + ZEN 40&#xa0;mg/kg), and H ASB/ZEN group (ASB 100&#xa0;mg/kg + ZEN 40&#xa0;mg/kg). The results showed that ZEN caused damage to the villous structure of the intestine and the ultrastructure of tight junctions, accompanied by a decrease in the number of goblet cells, a decrease in MUC-2 expression, an increase in serum LPS levels, a downregulation of tight junction protein expression, oxidative stress damage, and a disruption of the intestinal microbiota in faeces. Astilbin significantly ameliorated all these adverse effects. This investigation elucidates the mechanism by which ASB mitigates ZEN-induced intestinal injury via repairing the intestinal barrier. This study is the first to propose that astilbin (ASB) can alleviate zearalenone (ZEN)-induced intestinal injury by regulating the intestinal microbiota and repairing the intestinal barrier, thereby providing new mechanistic insights for the treatment of ZEN-induced enterotoxicity.</p>

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Protective effect of astilbin against intestinal barrier damage and gut microbiota dysbiosis in zearalenone-intoxicated mice

  • 期刊论文

  • 发表日期：

    2025年11月26日

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  • Zhaoyang Liu,
  • Shanshan Fei,
  • Yiding Liu,
  • Tianyu Han,
  • Yu Yang,
  • Guangliang Shi

摘要

Zearalenone (ZEN) is a stable, highly toxic compound that can cause multi-organ toxicity with prolonged exposure. Previous studies have demonstrated that ZEN can damage the physical barrier of the intestinal tract in animals. However, the relationship between ZEN-induced damage to the physical barrier of the intestinal tract in animals, oxidative stress, and the intestinal microbiota remains unclear. Astilbin (ASB) is a natural flavonoid renowned for its potent anti-inflammatory and antioxidant properties. However, whether ASB can alleviate ZEN-induced intestinal damage in mice remains unknown. In this study, we aimed to investigate whether ASB can alleviate ZEN-induced damage to the physical barrier and dysbiosis of the intestinal microbiota in mice. The study selected 36 male BALB/c mice aged 6 weeks, which were randomly divided into the CON group, the ZEN group (ZEN 40 mg/kg), the ASB group (ASB 100 mg/kg), the L ASB/ZEN group (ASB 25 mg/kg + ZEN 40 mg/kg), M ASB/ZEN group (ASB 50 mg/kg + ZEN 40 mg/kg), and H ASB/ZEN group (ASB 100 mg/kg + ZEN 40 mg/kg). The results showed that ZEN caused damage to the villous structure of the intestine and the ultrastructure of tight junctions, accompanied by a decrease in the number of goblet cells, a decrease in MUC-2 expression, an increase in serum LPS levels, a downregulation of tight junction protein expression, oxidative stress damage, and a disruption of the intestinal microbiota in faeces. Astilbin significantly ameliorated all these adverse effects. This investigation elucidates the mechanism by which ASB mitigates ZEN-induced intestinal injury via repairing the intestinal barrier. This study is the first to propose that astilbin (ASB) can alleviate zearalenone (ZEN)-induced intestinal injury by regulating the intestinal microbiota and repairing the intestinal barrier, thereby providing new mechanistic insights for the treatment of ZEN-induced enterotoxicity.