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<p>Lipopolysaccharide (LPS) is an immunostimulatory endotoxin component of the cell wall of Gram-negative bacteria. LPS correlates with unfavorable developmental consequences, such as preterm birth, fetal demise, teratogenic effects, and intrauterine growth restriction. Zinc is essential for embryogenesis, fetal development, and lactation. This study sought to assess the efficacy of zinc nanoparticles (Zn-NPs) in alleviating cerebellar toxicity caused by LPS in female rats and their offspring. Treatment of LPS-administered female rats with Zn-NPs led to a significant restoration of oxidative stress levels, as indicated by a substantial reduction in malondialdehyde and a marked improvement in superoxide dismutase catalase activity, and Glutathione content in the cerebellar tissues. A significant enhancement was observed in the lipid profiles (total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein) and neurotransmitters (serotonin and dopamine). This was accompanied by significant restoration in the histological and ultrastructural architecture of the cerebellar cortex damaged by LPS. Furthermore, the treatment of LPS-administered mothers with Zn-NPs significantly mitigated the neurodegenerative alterations generated by LPS, as demonstrated by the regulation of synaptophysin, chromogranin, and neuron-specific enolase. Conclusion: Zinc nanoparticles could potentially have a therapeutic role by mitigating cerebellar neurotoxicity caused by bacterial LPS during gestation by reducing oxidative stress and apoptosis.</p>

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The therapeutic potential of zinc-nanoparticles against the cerebellar neurotoxicity induced by bacterial lipopolysaccharides in female rats and their pups

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月4日

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  • Abd El-Fattah B. M. El-Beltagy,
  • Mai Eladad,
  • Karoline Kamel,
  • Hassan I. H. Elsayyad,
  • Amany Attallah

摘要

Lipopolysaccharide (LPS) is an immunostimulatory endotoxin component of the cell wall of Gram-negative bacteria. LPS correlates with unfavorable developmental consequences, such as preterm birth, fetal demise, teratogenic effects, and intrauterine growth restriction. Zinc is essential for embryogenesis, fetal development, and lactation. This study sought to assess the efficacy of zinc nanoparticles (Zn-NPs) in alleviating cerebellar toxicity caused by LPS in female rats and their offspring. Treatment of LPS-administered female rats with Zn-NPs led to a significant restoration of oxidative stress levels, as indicated by a substantial reduction in malondialdehyde and a marked improvement in superoxide dismutase catalase activity, and Glutathione content in the cerebellar tissues. A significant enhancement was observed in the lipid profiles (total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein) and neurotransmitters (serotonin and dopamine). This was accompanied by significant restoration in the histological and ultrastructural architecture of the cerebellar cortex damaged by LPS. Furthermore, the treatment of LPS-administered mothers with Zn-NPs significantly mitigated the neurodegenerative alterations generated by LPS, as demonstrated by the regulation of synaptophysin, chromogranin, and neuron-specific enolase. Conclusion: Zinc nanoparticles could potentially have a therapeutic role by mitigating cerebellar neurotoxicity caused by bacterial LPS during gestation by reducing oxidative stress and apoptosis.