在小鼠大脑中[a]皮林诱导的诺亚 adrenoergic轴突退化的炎症反应的作用
Yousra Reda1, Cai Zong2, Akane Ikoma2
1Department of Occupational and Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda 278-8510, Japan; Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, Egypt.
Toxicology letters
|September 29, 2025
概括
环境污染物[a]烯 (B[a]P) 引起神经毒性和神经炎症. 天然化合物硫福拉 (SFN) 保护了小鼠的B[a]P诱导的神经退行和脑部炎症.
科学领域:
- 神经科学是一个神经科学.
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
背景情况:
- 环境污染,特别是多环芳 (PAH),如甲 (B[a]P),与神经毒性和神经退行性疾病有关.
- 暴露于B[a]P与降低诺阿德仁基轴突密度和增加大脑中的炎症性细胞因子有关.
研究的目的:
- 为了调查B[a]P是否通过大脑炎症反应诱导神经退行.
- 为了确定抗氧化和抗炎化合物硫福拉 (SFN) 是否可以防止B[a]P诱导的神经毒性.
主要方法:
- 成年雄性小鼠通过喉吸收每周暴露在不同剂量的B[a]P中,并每天用SFN治疗4周.
- 神经毒性通过检查海马区域的诺亚腺激素轴突密度和Iba-1微质染色来评估.
- 对脑组织进行了包括NF-κB和Il-6在内的基因表达分析.
主要成果:
- 暴露于B[a]P导致大脑重量增加和神经毒性影响,包括降低诺亚上腺素轴突密度和海马中的微质激活.
- 施用SFN可以抵消B[a]P诱导的神经毒性,减轻大脑体重增加,轴突退化和微质激活.
- SFN抑制了由B[a]P诱导的关键炎症标志物NF-κB和Il-6的上调.
结论:
- 在小鼠海马体中,SFN有效地保护B[a]P诱导的神经炎症和轴突退化.
- 这些发现表明,B[a]P诱导的神经退行症通过大脑的炎症途径进行介导.
- SFN显示出作为治疗剂对环境毒素诱导的神经毒性的潜力.
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