噪声与微波复合暴露对小鼠海马结构和功能的影响及其机制OA

[Background]Co-exposure to noise and microwave radiation occurs frequently.The central ner-vous system has been identified as a sensitive target organ for both noise and microwave exposure individually,and the underlying mechanisms remain poorly understood.The specific biological effects resulting from co-exposure to these two factors have yet to be fully elucidated. [Objective]To clarify the effects of co-exposure to noise and microwave on neurobehavior and hippocampal tissue structure,and to explore the underlying mechanism through the assessment of serum cytokines. [Methods]C57BL/6N mice were selected and randomly assigned to a blank control group,a noise group,a microwave group,and a com-bined noise&microwave exposure group.To establish the exposure models,the noise group was subjected to broadband noise at 100 dB for 2 h,while the microwave group received radiation at a central frequency of 9.375 GHz with an average power density of 12 mW·cm-2 and a specific absorption rate of 2.58 W·kg-1 for 15 min.Open field and tail suspension tests assessed anxiety-like emotional behaviour;novel object recognition and Y-maze tests evaluated cognitive function.Histological changes in hippocampal tissue were ex-amined using haematoxylin and eosin(HE)staining,and Nissl staining under light microscopy.Serum cytokine levels were measured using radioimmunoassay and enzyme-linked immunosorbent assay(ELISA). [Results]After 3 d of exposure,the noise,microwave,and combined exposure groups showed significant reductions in exploration fre-quency,duration,and distance within the central zone of the open field test compared to the control group(P<0.01);the combined ex-posure group exhibited increased ratios of peripheral-to-central exploration time and distance(P<0.05).After 7 d of exposure,compared with the control group,the noise group maintained a decrease in central zone exploration time(P<0.01),while the combined exposure group showed persistent decline across all central zone metrics(P<0.05)and elevated peripheral-to-central ratios(P<0.05);compared to the microwave group,the combined exposure group showed significant less time in the central zone(P<0.05)and higher peripheral-to-central ratios(P<0.05).Regarding behaviour and cognition,compared with the control group,the combined exposure group showed increased immobility time in the tail suspension test after 3 d of exposure(P<0.01).At this interval,all exposure groups demonstrated reduced frequency and duration of novel object recognition(P<0.05),with the combined exposure group showing a marked decrease in novel arm exploration time(P<0.01).After 7 d of exposure,compared with the control group,the noise group showed reduced novel object recognition frequency(P<0.05),and both the noise and microwave groups exhibited decreased novel arm exploration time(P<0.05).Pathological alterations including an increased number of hyperchromatic nuclei and depleted Nissl bodies were observed in the CA3 and DG regions across all exposure groups with the most severe lesions observed in the combined exposure group.Serum levels of central nervous system-specific protein β(S-100β),glial fibrillary acidic protein(GFAP),and corticosterone(CORT)were significantly el-evated in all exposure groups compared with the control group(P<0.05).Aquaporin-4(AQP4)levels increased in the combined exposure group(P<0.05),while CXC chemokine ligand 10(CXCL10)levels rose in both the noise and combined groups compared with the control group(P<0.05).Specifically,S-100β and CXCL10 levels in the combined exposure group were higher than those in the microwave group(P<0.05);moreover,levels of S-100β,GFAP,CORT,AQP 4,and CXCL10 in the combined exposure group were significantly higher than those in the noise group(P<0.05). [Conclusion]Combined exposure to noise and microwave radiation induces pathological changes in the hippocampus of mice,increases levels of serum stress hormones and neuro-specific biomarkers.These impairments are more severe than those observed following single-factor exposure.The underlaying mechanism may be related to systemic stress response,neuronal damage,astrocyte activation,and changes in blood-brain barrier permeability,leading to emotional behavioral abnormalities and cognitive decline.