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Rationale <p>Memory decline (MD) and anxiety/depression-like behavior (ADB) are multisystem diseases involving gastrointestinal and microbiota dysbiosis. Long-term exposure to arsenic (As) has been shown to induce MD and ADB; however, the underlying mechanisms remain unknown. Research findings suggest that taurine exhibits protective effects by regulating gut microbiota composition.</p> Objective <p>To investigate the effects of taurine on alterations in gut microbiota, serum metabolites, brain tissue metabolites, and brain peptides in As-induced MD and ADB mouse models.</p> Results <p>Behavioral and immunohistochemical experiments revealed that As exposure caused abnormal activation and neuronal loss in the hippocampus and induced digestive system dysfunction in the MD and ADB mouse models. Mice with As-induced MD and ADB exhibited elevated abundances of Firmicutes and Parabasilia and significantly reduced abundances of Firmicutes A and Bacteroidetes. Additionally, differentially expressed metabolites related to antioxidant stress were significantly downregulated in the mouse models of MD and ADB. Moreover, the relative abundances of <i>Lawsonibacter</i>, <i>Dysosmobacter</i>, and <i>acetatifactor</i> were significantly correlated with differentially expressed metabolites related to antioxidant stress in mice with As-induced MD and ADB. Importantly, the expression patterns of receptor-associated proteins and antioxidant defense enzymes were significantly altered in mice with As-induced MD and ADB. Notably, taurine supplementation prevented the development of As-induced MD and ADB by inhibiting alterations in the gut microbiota and dysregulation of oxidative stress.</p> Conclusions <p>Taurine intervention inhibits As-induced alterations in the gut microbiota and ameliorates oxidative stress in brain tissues, thereby preventing the development of MD and ADB.</p>

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Taurine attenuates arsenic-induced neurotoxicity through modulation of gut microbiota structure

  • 期刊论文

  • 发表日期：

    2026年2月19日

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  • Haonan Zhang,
  • Wenjin Qiao,
  • Dapeng Tai,
  • Yuan Lv,
  • Hongyi Qi

摘要

Rationale

Memory decline (MD) and anxiety/depression-like behavior (ADB) are multisystem diseases involving gastrointestinal and microbiota dysbiosis. Long-term exposure to arsenic (As) has been shown to induce MD and ADB; however, the underlying mechanisms remain unknown. Research findings suggest that taurine exhibits protective effects by regulating gut microbiota composition.

Objective

To investigate the effects of taurine on alterations in gut microbiota, serum metabolites, brain tissue metabolites, and brain peptides in As-induced MD and ADB mouse models.

Results

Behavioral and immunohistochemical experiments revealed that As exposure caused abnormal activation and neuronal loss in the hippocampus and induced digestive system dysfunction in the MD and ADB mouse models. Mice with As-induced MD and ADB exhibited elevated abundances of Firmicutes and Parabasilia and significantly reduced abundances of Firmicutes A and Bacteroidetes. Additionally, differentially expressed metabolites related to antioxidant stress were significantly downregulated in the mouse models of MD and ADB. Moreover, the relative abundances of Lawsonibacter, Dysosmobacter, and acetatifactor were significantly correlated with differentially expressed metabolites related to antioxidant stress in mice with As-induced MD and ADB. Importantly, the expression patterns of receptor-associated proteins and antioxidant defense enzymes were significantly altered in mice with As-induced MD and ADB. Notably, taurine supplementation prevented the development of As-induced MD and ADB by inhibiting alterations in the gut microbiota and dysregulation of oxidative stress.

Conclusions

Taurine intervention inhibits As-induced alterations in the gut microbiota and ameliorates oxidative stress in brain tissues, thereby preventing the development of MD and ADB.