长期暴露于PM10会通过加剧海马氧化应激引起类似焦虑的行为
Jie Cheng1, Jian Sun2, Rui Niu3
1Department of Pharmacology, School of Basic Medical Sciences, Health Science Center, Xi'an Jiaotong University, Xi'an, 710061, China.
Free radical biology & medicine
|March 8, 2024
概括
暴露于颗粒物 (PM10) 在老鼠和人类中引发类似焦虑的行为. 这可能与氧化应激和海马体中抑制的抗氧化路径有关.
科学领域:
- 环境健康 环境健康
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
背景情况:
- 吸入颗粒物 (PM10) 是一个与各种健康问题有关的重大环境问题.
- 暴露在PM10和类似焦虑的行为之间的关系,以及其潜在的机制,仍然没有得到充分的研究.
研究的目的:
- 为了研究PM10暴露的行为和神经效应.
- 确定与PM10吸入相关的潜在毒理机制,包括氧化应激和海马变化.
主要方法:
- 鼠被内灌注PM10 (15毫克/公斤和30毫克/公斤) 八周.
- 分析了行为测试 (开放场,升高加迷宫),氧化应激标记,海马体形态和蛋白质表达.
- 还收集了人类在污染条件下对焦虑的问卷数据.
主要成果:
- 在老鼠中,暴露于PM10引起了显著的焦虑类行为.
- 观察到全血粘度增加,海马神经元损伤和氧化应激 (SOD和MDA升高).
- 观察到抗氧化蛋白的表达减少,包括Nrf2,SOD1和血氧酶1,这表明Nrf2/Keap1-SOD1通路被抑制.
结论:
- 吸入PM10可以诱导类似焦虑的行为和神经毒性.
- 这些发现表明,PM10诱导的焦虑可能是由氧化应激和抑制Nrf2/Keap1-SOD1抗氧化途径的介导.
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