Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice

BackgroundEnvironmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. ObjectiveTo explore the cognitive impairment induced by noise exposure during sleep in mice and possibl...

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Main Authors: Yiming FU, Xinyao ZHANG, Xiaojun SHE, Yingwen ZHU, Honglian YANG, Xiujie GAO, Bo FU, Bo CUI
Format: Article
Language:English
Published: Editorial Committee of Journal of Environmental and Occupational Medicine 2024-02-01
Series:环境与职业医学
Subjects:
Online Access:http://www.jeom.org/article/cn/10.11836/JEOM23198
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author Yiming FU
Xinyao ZHANG
Xiaojun SHE
Yingwen ZHU
Honglian YANG
Xiujie GAO
Bo FU
Bo CUI
author_facet Yiming FU
Xinyao ZHANG
Xiaojun SHE
Yingwen ZHU
Honglian YANG
Xiujie GAO
Bo FU
Bo CUI
author_sort Yiming FU
collection DOAJ
description BackgroundEnvironmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. ObjectiveTo explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. MethodsTwenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. ResultsAfter noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). ConclusionNoise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.
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spelling doaj.art-83c65a98f8a34db8861756d950dbf1002024-03-07T05:27:39ZengEditorial Committee of Journal of Environmental and Occupational Medicine环境与职业医学2095-99822024-02-0141211912410.11836/JEOM2319823198Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in miceYiming FU0Xinyao ZHANG1Xiaojun SHE2Yingwen ZHU3Honglian YANG4Xiujie GAO5Bo FU6Bo CUI7Institute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaInstitute of Environmental and Operational Medicine, Academy of Military Medical Sciences, Academy of Military Sciences, Tianjin 300050, ChinaBackgroundEnvironmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. ObjectiveTo explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. MethodsTwenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. ResultsAfter noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). ConclusionNoise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.http://www.jeom.org/article/cn/10.11836/JEOM23198sleep phase noise exposureneuroinflammationcognitive impairmentbiological clock
spellingShingle Yiming FU
Xinyao ZHANG
Xiaojun SHE
Yingwen ZHU
Honglian YANG
Xiujie GAO
Bo FU
Bo CUI
Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
环境与职业医学
sleep phase noise exposure
neuroinflammation
cognitive impairment
biological clock
title Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
title_full Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
title_fullStr Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
title_full_unstemmed Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
title_short Effects of long-term noise exposure during sleep on cognitive function and biological clock-related mechanisms in mice
title_sort effects of long term noise exposure during sleep on cognitive function and biological clock related mechanisms in mice
topic sleep phase noise exposure
neuroinflammation
cognitive impairment
biological clock
url http://www.jeom.org/article/cn/10.11836/JEOM23198
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