Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field

Objective‍ ‍To investigate the protective effect and mechanism of heat acclimation (HA) on electromagnetic field (EMF) induced hippocampus neuron injury in mice. Methods‍ ‍Forty healthy BALB/c male mice (18~22 g, 7 weeks old) were randomly divided into 4 groups (n=10): Control group (Con), HA group...

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Main Authors: WANG Zeze, YANG Xuesen, WANG Ying
Format: Article
Language:zho
Published: Editorial Office of Journal of Army Medical University 2025-04-01
Series:陆军军医大学学报
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Online Access:https://aammt.tmmu.edu.cn/html/202408087.html
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author WANG Zeze
WANG Zeze
YANG Xuesen
YANG Xuesen
WANG Ying
WANG Ying
author_facet WANG Zeze
WANG Zeze
YANG Xuesen
YANG Xuesen
WANG Ying
WANG Ying
author_sort WANG Zeze
collection DOAJ
description Objective‍ ‍To investigate the protective effect and mechanism of heat acclimation (HA) on electromagnetic field (EMF) induced hippocampus neuron injury in mice. Methods‍ ‍Forty healthy BALB/c male mice (18~22 g, 7 weeks old) were randomly divided into 4 groups (n=10): Control group (Con), HA group (34 ℃, 30 d), EMF group (2 450 MHz, 20 min/d, 4 weeks) and HA+EMF group (HA preconditioning+EMF). Sucrose preference test was performed to evaluate sucrose preference levels of mice in each group. Tail suspension test and forced swimming test were utilized to observe the immobility time. Morris water maze test was conducted to determine the learning and memory capabilities. Pathological changes in the hippocampus were observed with HE staining. Immunohistochemical assay for Iba1 (marker of microglia), CD68 (marker of pro-inflammatory phenotype) and CD206 (marker of anti-inflammatory phenotype) were used to detect the number and activation phenotype of microglia in the hippocampus. ELISA was applied to measure the levels of TNF-α, IL-1β, TGF-β and IL-10 in the hippocampus of each group. Western blotting was performed to determine the protein levels of HSP70 in the hippocampus. Results‍ ‍As compared with the Con group, the EMF group showed a decreased preference for sucrose (P<0.05), prolonged immobile time in the tail suspension test (P<0.01) as well as in the forced swimming test (P<0.01), extented escape latency on the 7th day (P<0.01), and a decreased time of crossing the platform (P<0.05). EMF exposure resulted in that the hippocampal neurons were in disordered arrangement, loose structure and irregular morphology, with swollen cytoplasm and condensed nuclei, swollen and more microglial cells in the hippocampus (P<0.01), and enhanced relative fluorescence intensity of CD68 (P<0.01), but not in CD206 fluorescence intensity (P=0.885). All these findings suggested that activated microglia predominantly exhibited a pro-inflammatory M1 phenotype during this phase. In the hippocampus, the levels of TNF-α and IL-1β were significantly increased, while the levels of IL-10 and TGF-β were significantly decreased (P<0.01).HA treatment reversed the conditions induced by EMF exposure, including better preference for sucrose (P<0.01), shorten immobile time in tail suspension test (P<0.05) and forced swimming test (P<0.01), less escape latency on the 7th day (P<0.01), and improved hippocampal cell injuries. Compared with the Con group, there were more microglial cells in the hippocampus in the HA+EMF group, with increased relative fluorescence intensity of M2 phenotype marker CD206 (P<0.01) and decreased CD68 fluorescence intensity (P<0.01). HA treatment also significantly decreased the expression of TNF-α and IL-1β levels (P<0.01), increased the expression of IL-10 and TGF-β (P<0.01), and elevated the protein level of HSP70 (P<0.01) when compared with the EMF group. Conclusion‍ ‍HA may ameliorate EMF-induced hippocampus neurons injury in mice by altering the phenotype of activated microglia and inhibiting inflammatory responses.
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spelling doaj-art-6df292bdb3ad457392f383d7cf92d74a2025-08-20T03:10:06ZzhoEditorial Office of Journal of Army Medical University陆军军医大学学报2097-09272025-04-0147762963810.16016/j.2097-0927.202408087Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic fieldWANG Zeze0WANG Zeze1YANG Xuesen2YANG Xuesen3WANG Ying4WANG Ying5Department of Tropical Medicine, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, ChinaKey Laboratory of Extreme Environmental Medicine of Ministry of Education, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, ChinaDepartment of Tropical Medicine, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, China Key Laboratory of Extreme Environmental Medicine of Ministry of Education, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, ChinaDepartment of Tropical Medicine, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, ChinaKey Laboratory of Extreme Environmental Medicine of Ministry of Education, (Cultivation), Faculty of Military Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, ChinaObjective‍ ‍To investigate the protective effect and mechanism of heat acclimation (HA) on electromagnetic field (EMF) induced hippocampus neuron injury in mice. Methods‍ ‍Forty healthy BALB/c male mice (18~22 g, 7 weeks old) were randomly divided into 4 groups (n=10): Control group (Con), HA group (34 ℃, 30 d), EMF group (2 450 MHz, 20 min/d, 4 weeks) and HA+EMF group (HA preconditioning+EMF). Sucrose preference test was performed to evaluate sucrose preference levels of mice in each group. Tail suspension test and forced swimming test were utilized to observe the immobility time. Morris water maze test was conducted to determine the learning and memory capabilities. Pathological changes in the hippocampus were observed with HE staining. Immunohistochemical assay for Iba1 (marker of microglia), CD68 (marker of pro-inflammatory phenotype) and CD206 (marker of anti-inflammatory phenotype) were used to detect the number and activation phenotype of microglia in the hippocampus. ELISA was applied to measure the levels of TNF-α, IL-1β, TGF-β and IL-10 in the hippocampus of each group. Western blotting was performed to determine the protein levels of HSP70 in the hippocampus. Results‍ ‍As compared with the Con group, the EMF group showed a decreased preference for sucrose (P<0.05), prolonged immobile time in the tail suspension test (P<0.01) as well as in the forced swimming test (P<0.01), extented escape latency on the 7th day (P<0.01), and a decreased time of crossing the platform (P<0.05). EMF exposure resulted in that the hippocampal neurons were in disordered arrangement, loose structure and irregular morphology, with swollen cytoplasm and condensed nuclei, swollen and more microglial cells in the hippocampus (P<0.01), and enhanced relative fluorescence intensity of CD68 (P<0.01), but not in CD206 fluorescence intensity (P=0.885). All these findings suggested that activated microglia predominantly exhibited a pro-inflammatory M1 phenotype during this phase. In the hippocampus, the levels of TNF-α and IL-1β were significantly increased, while the levels of IL-10 and TGF-β were significantly decreased (P<0.01).HA treatment reversed the conditions induced by EMF exposure, including better preference for sucrose (P<0.01), shorten immobile time in tail suspension test (P<0.05) and forced swimming test (P<0.01), less escape latency on the 7th day (P<0.01), and improved hippocampal cell injuries. Compared with the Con group, there were more microglial cells in the hippocampus in the HA+EMF group, with increased relative fluorescence intensity of M2 phenotype marker CD206 (P<0.01) and decreased CD68 fluorescence intensity (P<0.01). HA treatment also significantly decreased the expression of TNF-α and IL-1β levels (P<0.01), increased the expression of IL-10 and TGF-β (P<0.01), and elevated the protein level of HSP70 (P<0.01) when compared with the EMF group. Conclusion‍ ‍HA may ameliorate EMF-induced hippocampus neurons injury in mice by altering the phenotype of activated microglia and inhibiting inflammatory responses. https://aammt.tmmu.edu.cn/html/202408087.html‍heat acclimationelectromagnetic fieldhippocampus neuronsinflammatory responsesheat shock protein 70
spellingShingle WANG Zeze
WANG Zeze
YANG Xuesen
YANG Xuesen
WANG Ying
WANG Ying
Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
陆军军医大学学报
‍heat acclimation
electromagnetic field
hippocampus neurons
inflammatory responses
heat shock protein 70
title Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
title_full Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
title_fullStr Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
title_full_unstemmed Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
title_short Protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
title_sort protective effect and mechanism of heat acclimation on hippocampus neuron injury in mice after exposure to electromagnetic field
topic ‍heat acclimation
electromagnetic field
hippocampus neurons
inflammatory responses
heat shock protein 70
url https://aammt.tmmu.edu.cn/html/202408087.html
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