Department of Medical Imaging, The 960th Hospital of Joint Logistics Support Force of PLA, Shandong Province, PR China.
Department of Spinal Cord Injury and Repair, Trauma and Orthopedics Institute of Chinese PLA, The 960th Hospital of Joint Logistics Support Force of PLA, Shandong Province, PR China; Institute of Military Cognitive and Brain Sciences, Academy of Military Medical Sciences, Beijing, 100850, PR China.
Chemosphere. 2021 Jul;274:129739. doi: 10.1016/j.chemosphere.2021.129739. Epub 2021 Jan 22.
To our knowledge, little evidence is available about effects of aircraft noise (AN), a non-chemical stressor, on cognitive function. Again, it is unknown whether or not the heat stress (HS)-induced cognitive deficits can be exacerbated by AN. The adult male mice were assigned to four groups: group 1 mice exposed to non-HS (24-26 °C 2 h daily for 4 consecutive days) and white noise (WN) (2 h daily for 4 consecutive days), group 2 mice exposed to WN and HS (32-34 °C 2 h daily for 4 consecutive days), group 3 mice exposed to AN and non-HS (2 h daily for 4 consecutive days) and group 4 mice exposed to AN and HS (2 h daily for consecutive 4 days). Cognitive function were determined by passive avoidance, Y-maze, Morris water maze, and novel object recognition tests. Gut barrier and blood-brain-barrier (BBB) permeability, upload of lipopolysaccharide (LPS) translocation, systemic and central inflammation, and stress reactions were examined. Heat stressed mice displayed both increased stress reactions and learning and memory loss. Heat stress also caused gut barrier hyperpermeability, increased upload of LPS translocation, systemic inflammation, BBB disruption and hippocampal neuroinflammation. Aircraft noise stressed mice did not display systemic inflammation but caused gut barrier hyperpermeability, increased upload of LPS translocation, increased stress reactions, BBB disruption, hippocampal neuroinflammation and cognitive deficits. Aircraft noise exposure further exacerbated the heat stress-induced cognitive deficits and its complications. Our data suggest that AN, like HS, causes cognitive impairments via similar mechanisms in male mice.
据我们所知，关于飞机噪声（AN）这种非化学应激源对认知功能的影响，几乎没有证据。同样，也不知道热应激（HS）引起的认知缺陷是否会因 AN 而加剧。雄性成年小鼠被分配到四个组：第 1 组小鼠暴露于非 HS（24-26°C，每天 2 小时，连续 4 天）和白噪声（WN）（每天 2 小时，连续 4 天），第 2 组小鼠暴露于 WN 和 HS（32-34°C，每天 2 小时，连续 4 天），第 3 组小鼠暴露于 AN 和非 HS（每天 2 小时，连续 4 天），第 4 组小鼠暴露于 AN 和 HS（每天 2 小时，连续 4 天）。通过被动回避、Y 迷宫、莫里斯水迷宫和新物体识别测试来确定认知功能。检查肠道屏障和血脑屏障（BBB）通透性、脂多糖（LPS）易位的上传、全身和中枢炎症以及应激反应。热应激小鼠表现出应激反应增加和学习记忆丧失。热应激还导致肠道屏障通透性增加、LPS 易位上传增加、全身炎症、BBB 破坏和海马神经炎症。飞机噪声应激小鼠没有显示出全身炎症，但导致肠道屏障通透性增加、LPS 易位上传增加、应激反应增加、BBB 破坏、海马神经炎症和认知缺陷。飞机噪声暴露进一步加剧了热应激引起的认知缺陷及其并发症。我们的数据表明，与 HS 一样，AN 通过类似的机制导致雄性小鼠认知障碍。
