Objective:To analyze the differential protein expression in the hypothalamus of PCPA-induced in-somnia rat models using proteomics,and to explore the protein interaction networks involved in the pathogenesis of in-somnia.Methods:SD rats were randomly divided into blank group,Model A group,and Model B group.Except for the blank group,all groups were modeled with PCPA.In the Model A group,the hypothalamus was harvested immedi-ately after successful modeling,while in the blank and Model B groups,the hypothalamus was harvested after 7 days,allowing PCPA effects to subside.Proteomics technology was used to detect differential protein expression in the hypo-thalamus of each group.Proteins with differential expression levels greater than 1.5-fold(upregulated or downregulat-ed)were identified and analyzed for interaction relationships.Results:Sodium pentobarbital righting reflex tests showed that sleep latency was significantly prolonged(P＜0.01)and sleep duration significantly shortened(P＜0.01)in both Model A and Model B groups compared to the blank group.Spontaneous activity tests revealed an increased number of paw lifts in the Model A and Model B groups compared to the blank group(P＜0.05).Protein interaction network analysis identified 16 key proteins in the network between the Model A and blank groups,among which Map1(T-kininogen 1),Mfge8(Lactadherin),and P4hb(Protein disulfide-isomerase)were closely related to insomnia.In the network between the Model B and Model A groups,12 key proteins were identified,including Apoa1(Apoli-poprotein A-I),Mfge8(Lactadherin),Sympk(Symplekin),and Plg(Plasminogen),which were strongly associated with insomnia.Conclusion:Protein interaction network analysis of the hypothalamus in PCPA-induced rat models suggests that the occurrence and progression of insomnia may be related to stress responses of the HPA axis,neurode-generative protection,vascular endothelial cells,endocrine regulation,immune system balance,learning and memory abilities,and aging.
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