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Negative air ion exposure ameliorates depression-like behaviors induced by chronic mild stress in mice

The presence of negative air ions (NAI) is suggested to be a beneficial factor in improving psychological status and used in treating depression as an alternative approach. However, more biological evidence from animal models is needed to ensure the effects of NAI on the mood regulation, through whi...

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Detalles Bibliográficos
Autores principales: Hu, Yun-Qing, Niu, Ting-Ting, Xu, Jian-ming, Peng, Li, Sun, Qing-Hua, Huang, Ying, Zhou, Ji, Ding, Yu-Qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9464145/
https://www.ncbi.nlm.nih.gov/pubmed/35411516
http://dx.doi.org/10.1007/s11356-022-20144-x
Descripción
Sumario:The presence of negative air ions (NAI) is suggested to be a beneficial factor in improving psychological status and used in treating depression as an alternative approach. However, more biological evidence from animal models is needed to ensure the effects of NAI on the mood regulation, through which can facilitate identification of possible underlying mechanisms. In this study, the chronic mild stress (CMS) protocol was used to induce depressive-like behaviors in mice, and the effects of NAI exposure on CMS-induced depression-like behaviors were examined. Thirty-day NAI exposure prevented the CMS-induced depression-like behaviors as shown by the restoration of sucrose preference and reduced immobility time in the tail suspension test. In addition, the elevation of serous corticosterone was present in CMS-treated mice but not existed in those with the NAI exposure. Furthermore, we observed altered ratios of some cytokines secreted by type 1 T helper (Th1) cells and Th2 cells in CMS-treated mice, but it could be restored after NAI exposure. In conclusion, NAI intervention is able to ameliorate CMS-induced depression-like behaviors in mice, and this effect is associated with the alteration of corticosterone and functional rebalance between Th1 and Th2 cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11356-022-20144-x.