Exposure to ambient dusty particulate matter impairs spatial memory and hippocampal LTP by increasing brain inflammation and oxidative stress in rats

氧化应激 海马结构 神经科学 海马体 微粒 长时程增强 内科学 医学 炎症 心理学 生物 生态学 受体
作者
Somayeh Hajipour,Yaghoob Farbood,Mohammad Kazem Gharib-Naseri,Gholamreza Goudarzi,Mohammad Rashno,Heidar Maleki,Nima Bakhtiari,Ali Nesari,Seyed Esmaeil Khoshnam,Mahin Dianat,Behjat Sarkaki,Alireza Sarkaki
出处
期刊:Life Sciences [Elsevier BV]
卷期号:242: 117210-117210 被引量:58
标识
DOI:10.1016/j.lfs.2019.117210
摘要

Exposure of healthy subjects to ambient airborne dusty particulate matter (PM) causes brain dysfunction. This study aimed to investigate the effect of sub-chronic inhalation of ambient PM in a designed special chamber to create factual dust storm (DS) conditions on spatial cognition, hippocampal long-term potentiation (LTP), inflammatory cytokines, and oxidative stress in the brain tissue.Adult male Wistar rats (250-300 g) were randomly divided into four groups: Sham (clean air, the concentration of dusty PM was <150 μg/m3), DS1 (200-500 μg/m3), DS2 (500-2000 μg/m3) and DS3 (2000-8000 μg/m3). Experimental rats were exposed to clean air or different sizes and concentrations of dust PM storm for four consecutive weeks (exposure was during 1-4, 8-11, 15-16 and 20-23 days, 30 min, twice daily) in a real-ambient dust exposure chamber. Subsequently, cognitive performance, hippocampal LTP, blood-brain barrier (BBB) permeability and brain edema of the animals evaluated. As well as, inflammatory cytokines and oxidative stress indexes in the brain tissue measured using ELISA assays.Exposing to dust PM impaired spatial memory (p < 0.001), hippocampal LTP (p < 0.001). These disturbances were in line with the severe damage to respiratory system followed by disruption of BBB integrity (p < 0.001), increased brain edema (p < 0.001), inflammatory cytokines (p < 0.001) excretion and oxidative stress (p < 0.001) in brain tissue.Our study showed that exposure to ambient dust PM increased brain edema and BBB permeability, induced memory impairment and hippocampal LTP deficiency by increasing the inflammatory responses and oxidative stress in the brain of the rats.

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