Objective:To identify core genes with co-expression trends in the suprachiasmatic nucleus (SCN) and lateral habenula (LHb) through miRNA sequencing, and to explore the molecular mechanisms underlying the onset and progress of sleep disturbances in depression.Methods:A rat model of depression with sleep disturbances was established. Behavioral assessments were conducted using the pentobarbital-induced sleep test, sucrose water consumption test, and open field test. Differentially expressed genes (DEGs) in the SCN and LHb of model rats were analyzed using biological replicates with the limma package and DESeq2 software. Gene ontology (GO), KEGG, Reactome pathway-gene set enrichment analysis (GSEA) were performed on the DEGs.Co-expression networks and protein-protein interaction (PPI) networks were constructed using R and Cytoscape software for further screening of genes with potential regulatory roles.Results:After modeling, the sleep latency in the model group ((679.88±350.05) s) was longer than that in the normal group ((316.25±87.35) s) ( t=-2.851, P=0.022), while the sleep duration in the model group ((33.13±8.41) min) was shorter than that in the normal group ((69.72±25.11) min) ( t=3.907, P=0.004). Additionally, the model group exhibited lower sucrose water consumption, horizontal movement counts, and vertical movement counts compared to the normal group (all P<0.05). Differential expression gene analysis showed, in the SCN, 379 genes were upregulated and 132 genes were downregulated, with the top five most significantly differentially expressed genes being Sec61g, Cox6b1, Ephx2, Thrsp, and Pak2. In the LHb, 1 657 genes were upregulated and 1 737 were downregulated, with the top five most significantly differentially expressed genes being Mrpl32, Mrpl20, Mrpl27, Celsr2, and Uba52. Biological pathways enriched in the SCN were mainly associated with the positive regulation of responses to external and biological stimuli. In contrast, pathways enriched in the LHb were related to neurotransmitter level regulation, developmental growth, neurotransmitter transport, and processes such as learning and memory. Co-expression network analysis identified 864 interactions involving 100 nodes in the SCN and 524 interactions involving 99 nodes in the LHb. Conclusion:The biological functions and signaling pathways of the suprachiasmatic nucleus and lateral habenula are different in the occurrence and development of depression with sleep disturbance, and the significantly differentially expressed genes may play an important role.

Objective:To identify core genes with co-expression trends in the suprachiasmatic nucleus (SCN) and lateral habenula (LHb) through miRNA sequencing, and to explore the molecular mechanisms underlying the onset and progress of sleep disturbances in depression.Methods:A rat model of depression with sleep disturbances was established. Behavioral assessments were conducted using the pentobarbital-induced sleep test, sucrose water consumption test, and open field test. Differentially expressed genes (DEGs) in the SCN and LHb of model rats were analyzed using biological replicates with the limma package and DESeq2 software. Gene ontology (GO), KEGG, Reactome pathway-gene set enrichment analysis (GSEA) were performed on the DEGs.Co-expression networks and protein-protein interaction (PPI) networks were constructed using R and Cytoscape software for further screening of genes with potential regulatory roles.Results:After modeling, the sleep latency in the model group ((679.88±350.05) s) was longer than that in the normal group ((316.25±87.35) s) ( t=-2.851, P=0.022), while the sleep duration in the model group ((33.13±8.41) min) was shorter than that in the normal group ((69.72±25.11) min) ( t=3.907, P=0.004). Additionally, the model group exhibited lower sucrose water consumption, horizontal movement counts, and vertical movement counts compared to the normal group (all P<0.05). Differential expression gene analysis showed, in the SCN, 379 genes were upregulated and 132 genes were downregulated, with the top five most significantly differentially expressed genes being Sec61g, Cox6b1, Ephx2, Thrsp, and Pak2. In the LHb, 1 657 genes were upregulated and 1 737 were downregulated, with the top five most significantly differentially expressed genes being Mrpl32, Mrpl20, Mrpl27, Celsr2, and Uba52. Biological pathways enriched in the SCN were mainly associated with the positive regulation of responses to external and biological stimuli. In contrast, pathways enriched in the LHb were related to neurotransmitter level regulation, developmental growth, neurotransmitter transport, and processes such as learning and memory. Co-expression network analysis identified 864 interactions involving 100 nodes in the SCN and 524 interactions involving 99 nodes in the LHb. Conclusion:The biological functions and signaling pathways of the suprachiasmatic nucleus and lateral habenula are different in the occurrence and development of depression with sleep disturbance, and the significantly differentially expressed genes may play an important role.

Objective To observe the change of coagulation function in chronic stress depression model rats and the effects of elec-troacupuncture (EA) on it. Methods A total of 32 Sprague-Dawley rats were randomly divided in control group (n=8), model group (n=8), EA group (n=8) and fluoxetine group (n=8) after a week of acclimation. The 21-day unpredictable mild stress combined with solitarily feed-ing was used to make the depression model in the latter three groups, meanwhile EA group and the fluoxetine group accepted EA and fluox-etine. They were measured the prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and fibrinogen (FIB). Serum levels of 6-keto-prostaglandin F1α(6-keto-PGF1α), P-selectin, thromboxane B2 (TXB2) were determined with enzyme-linked im-munoabsorbent assay. Results The cross and rear scores were significantly lower in the model group than in the control group (P<0.01). The scores increased in EA group and the fluoxetine group (P<0.01) compared with the model group. Compared with the control group, PT, APTT and TT decreased (P<0.01), FIB increased (P<0.05), the level of 6-keto-PGF1αdecreased, the level of P-selectin and TXB2 increased (P<0.01) in the model group. Compared with the model group, PT, APTT and TT increased (P<0.05), the level of 6-keto-PGF1αincreased (P<0.01), and the level of P-selectin and TXB2 decreased (P<0.05) in EA group and the fluoxetine group, and FIB decreased in EA group (P<0.05). Conclusion The chronic stress depression rats are impaired in the coagulation function and platelet activation, and can be allayed with electroacupuncture and fluoxetine.

Objective To explore the biological mechanisms of electroacupuncture (EA) for depression. Methods Forty male adult Sprague-Dawley rats were randomly divided into control group (n=8), model group (n=8), EA group (n=8) and fluoxetine group (n=8). Depressive models were established with lonely raising and chronic unpredictable mild stress. They were tested with Open-field Test, and the expression of phosphodiesterase 4 (PDE4)A and PDE4D in hippocampus was detected with RT-PCR. Results The cross and rear scores were significantly lower in the model group than in the control group (P<0.001), while it increased in the EA group and the fluoxetine group (P<0.001). Compared with the model group, the expression of PDE4A and PDE4D decreased in the EA group (P<0.001). Conclusion Electroacupuncture may relieve depression through inhibiting the expression of PDE4A and PDE4D.