Xiao-Jie Dai, Jun-Hua Liao, Yi Jia, Rui Cao, Mei-Ning Zhou
{"title":"噪音会促进阿尔茨海默病样病变和 DNA 损伤","authors":"Xiao-Jie Dai, Jun-Hua Liao, Yi Jia, Rui Cao, Mei-Ning Zhou","doi":"10.4103/nah.nah_26_24","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the mechanism by which noise contributes to the development of Alzheimer's disease (AD)-like lesions.</p><p><strong>Method: </strong>Male Wistar rats (24 months) were allocated into two groups (n = 6 per groups): a noise group exposed to 98 dB sound pressure-level white noise for 4 hours daily from 8:00 to 12:00 for 30 days, and a control group without noise exposure. The cognitive functions of the rats were assessed using new-object recognition and Morris water maze tests. Then, hippocampal tissues were collected, and the levels of amyloid β 1-42 (Aβ1-42), Aβ1-40, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB) were measured using enzyme-linked immunosorbent assay (ELISA). Protein expression was evaluated through Western blot.</p><p><strong>Results: </strong>Noise exposure significantly impaired cognitive and recognition abilities, increased the escape latency, and decreased the number of crossings through the platform quadrant intersection and the time spent in the target quadrant (P < 0.01). The new-object exploration and recognition index of the rats in the noise group markedly decreased (P < 0.01). ELISA results indicated increases in Aβ1-40 and Aβ1-42 levels and decreases in BDNF and TrkB levels in the rat hippocampus in the noise group (P < 0.01). Western blot analyses revealed that beta-site amyloid precursor protein (APP) cleaving enzyme 1, phosphorylated tau protein, gamma-H2A histone family, member X, checkpoint kinase 2, p53, and p21 were remarkably elevated in the noise group (P < 0.01).</p><p><strong>Conclusion: </strong>Chronic noise exposure can cause hippocampal genetic damage in aged rats, leading to cognitive disorders and the development of lesions similar to those observed in AD. Thus, noise is a potential risk factor for neurodegenerative disorders.</p>","PeriodicalId":19195,"journal":{"name":"Noise & Health","volume":"26 122","pages":"287-293"},"PeriodicalIF":1.3000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11539988/pdf/","citationCount":"0","resultStr":"{\"title\":\"Noise Exposure Promotes Alzheimer's Disease-Like Lesions and DNA Damage.\",\"authors\":\"Xiao-Jie Dai, Jun-Hua Liao, Yi Jia, Rui Cao, Mei-Ning Zhou\",\"doi\":\"10.4103/nah.nah_26_24\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>This study aimed to explore the mechanism by which noise contributes to the development of Alzheimer's disease (AD)-like lesions.</p><p><strong>Method: </strong>Male Wistar rats (24 months) were allocated into two groups (n = 6 per groups): a noise group exposed to 98 dB sound pressure-level white noise for 4 hours daily from 8:00 to 12:00 for 30 days, and a control group without noise exposure. The cognitive functions of the rats were assessed using new-object recognition and Morris water maze tests. Then, hippocampal tissues were collected, and the levels of amyloid β 1-42 (Aβ1-42), Aβ1-40, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB) were measured using enzyme-linked immunosorbent assay (ELISA). Protein expression was evaluated through Western blot.</p><p><strong>Results: </strong>Noise exposure significantly impaired cognitive and recognition abilities, increased the escape latency, and decreased the number of crossings through the platform quadrant intersection and the time spent in the target quadrant (P < 0.01). The new-object exploration and recognition index of the rats in the noise group markedly decreased (P < 0.01). ELISA results indicated increases in Aβ1-40 and Aβ1-42 levels and decreases in BDNF and TrkB levels in the rat hippocampus in the noise group (P < 0.01). Western blot analyses revealed that beta-site amyloid precursor protein (APP) cleaving enzyme 1, phosphorylated tau protein, gamma-H2A histone family, member X, checkpoint kinase 2, p53, and p21 were remarkably elevated in the noise group (P < 0.01).</p><p><strong>Conclusion: </strong>Chronic noise exposure can cause hippocampal genetic damage in aged rats, leading to cognitive disorders and the development of lesions similar to those observed in AD. 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Noise Exposure Promotes Alzheimer's Disease-Like Lesions and DNA Damage.
Objective: This study aimed to explore the mechanism by which noise contributes to the development of Alzheimer's disease (AD)-like lesions.
Method: Male Wistar rats (24 months) were allocated into two groups (n = 6 per groups): a noise group exposed to 98 dB sound pressure-level white noise for 4 hours daily from 8:00 to 12:00 for 30 days, and a control group without noise exposure. The cognitive functions of the rats were assessed using new-object recognition and Morris water maze tests. Then, hippocampal tissues were collected, and the levels of amyloid β 1-42 (Aβ1-42), Aβ1-40, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB) were measured using enzyme-linked immunosorbent assay (ELISA). Protein expression was evaluated through Western blot.
Results: Noise exposure significantly impaired cognitive and recognition abilities, increased the escape latency, and decreased the number of crossings through the platform quadrant intersection and the time spent in the target quadrant (P < 0.01). The new-object exploration and recognition index of the rats in the noise group markedly decreased (P < 0.01). ELISA results indicated increases in Aβ1-40 and Aβ1-42 levels and decreases in BDNF and TrkB levels in the rat hippocampus in the noise group (P < 0.01). Western blot analyses revealed that beta-site amyloid precursor protein (APP) cleaving enzyme 1, phosphorylated tau protein, gamma-H2A histone family, member X, checkpoint kinase 2, p53, and p21 were remarkably elevated in the noise group (P < 0.01).
Conclusion: Chronic noise exposure can cause hippocampal genetic damage in aged rats, leading to cognitive disorders and the development of lesions similar to those observed in AD. Thus, noise is a potential risk factor for neurodegenerative disorders.
Noise & HealthAUDIOLOGY & SPEECH-LANGUAGE PATHOLOGY-PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
CiteScore
2.10
自引率
14.30%
发文量
27
审稿时长
6-12 weeks
期刊介绍:
Noise and Health is the only International Journal devoted to research on all aspects of noise and its effects on human health. An inter-disciplinary journal for all professions concerned with auditory and non-auditory effects of occupational, environmental, and leisure noise. It aims to provide a forum for presentation of novel research material on a broad range of topics associated with noise pollution, its control and its detrimental effects on hearing and health. It will cover issues from basic experimental science through clinical evaluation and management, technical aspects of noise reduction systems and solutions to environmental issues relating to social and public health policy.