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<p>Microplastic (MPs) pollution is widespread in the environment and poses growing risks to food safety and human health. In a 60-day oral exposure study, male Swiss mice received MPs (10 mg/kg b.wt), and the neuroprotective potential of taurine (Tau, 200 mg/kg b.wt) was evaluated. MPs exposure induced pronounced anxiety-like behavior, evidenced by increased peripheral zone activity in the open field test (+ 81.1%) and elevated anxiety index in the elevated plus maze (+ 75.9%), along with significant memory and spatial learning impairments in the Y-maze (increased trials + 31.6% and latency + 75.2%). Neurochemically, MPs increased acetylcholinesterase (AChE) activity (+ 89.4%) while reducing dopamine (−29.4%) and γ-aminobutyric acid (GABA) (−17.9%) levels. MPs also triggered marked oxidative stress, as shown by elevated reactive oxygen species (+ 107.6%) and malondialdehyde (+ 249.0%), accompanied by reduced total antioxidant capacity (−26.2%). At the molecular level, MPs downregulated CREB1 (−82.2%) and BDNF (−80.2%) while markedly upregulating AKT1 (~ fivefold) and pro-inflammatory cytokines (TNF-α, IL-6, CXCL-10, and IL-1β; 5.2–7.2-fold). Histopathological analysis revealed severe neurodegenerative alterations across the cerebrum, hippocampus, and cerebellum. Tau co-treatment significantly ameliorated MPs’ induced neurotoxicity by reducing anxiety and memory deficits, lowering AChE activity (− 17.3%), restoring dopamine (+ 28.8%) and GABA (+ 14.2%) levels, attenuating oxidative stress (ROS −45.4% and MDA −44.7%), suppressing inflammatory gene expression (−51.0 to −68.1%), and partially normalizing CREB1 and BDNF expression (+239% and +240%, respectively). Collectively, these findings identify Tau as a promising natural neuroprotective agent against MPs’ induced neurotoxicity.</p>

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Taurine Mitigates Microplastic-Induced Neurotoxicity Through Modulation of Neurobehavior, Neurotransmitters, Oxidative Stress, and AKT-1/CREB-1/BDNF Signaling in Mice

  • 期刊论文

  • 发表日期：

    2026年1月1日

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  • Wafa S. Alansari,
  • Eman S. El-Shetry,
  • Badriyah S. Alotaibi,
  • Yasmina M. Abd-Elhakim,
  • Amany Abdel-Rahman Mohamed,
  • Enas N. Said,
  • Ahmed E. Noreldin,
  • Tarek Khamis,
  • Nawal Alsubaie,
  • Ayman A. Saleh

摘要

Microplastic (MPs) pollution is widespread in the environment and poses growing risks to food safety and human health. In a 60-day oral exposure study, male Swiss mice received MPs (10 mg/kg b.wt), and the neuroprotective potential of taurine (Tau, 200 mg/kg b.wt) was evaluated. MPs exposure induced pronounced anxiety-like behavior, evidenced by increased peripheral zone activity in the open field test (+ 81.1%) and elevated anxiety index in the elevated plus maze (+ 75.9%), along with significant memory and spatial learning impairments in the Y-maze (increased trials + 31.6% and latency + 75.2%). Neurochemically, MPs increased acetylcholinesterase (AChE) activity (+ 89.4%) while reducing dopamine (−29.4%) and γ-aminobutyric acid (GABA) (−17.9%) levels. MPs also triggered marked oxidative stress, as shown by elevated reactive oxygen species (+ 107.6%) and malondialdehyde (+ 249.0%), accompanied by reduced total antioxidant capacity (−26.2%). At the molecular level, MPs downregulated CREB1 (−82.2%) and BDNF (−80.2%) while markedly upregulating AKT1 (~ fivefold) and pro-inflammatory cytokines (TNF-α, IL-6, CXCL-10, and IL-1β; 5.2–7.2-fold). Histopathological analysis revealed severe neurodegenerative alterations across the cerebrum, hippocampus, and cerebellum. Tau co-treatment significantly ameliorated MPs’ induced neurotoxicity by reducing anxiety and memory deficits, lowering AChE activity (− 17.3%), restoring dopamine (+ 28.8%) and GABA (+ 14.2%) levels, attenuating oxidative stress (ROS −45.4% and MDA −44.7%), suppressing inflammatory gene expression (−51.0 to −68.1%), and partially normalizing CREB1 and BDNF expression (+239% and +240%, respectively). Collectively, these findings identify Tau as a promising natural neuroprotective agent against MPs’ induced neurotoxicity.