ArticleNature and science of sleep2026
Network Pharmacology-Based Elucidation of Gu's Anshen Decoction in Modulating TNF Signaling to Ameliorate Insomnia.
Article in Nature and science of sleep, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the therapeutic mechanisms of Gu's Anshen decoction (GAD) against insomnia (INS), focusing on the regulation of tumor necrosis factor (TNF)-mediated inflammatory pathways. Methods: Bioactive compounds and potential targets of GAD were identified via network pharmacology and constructed herb-compound-target interaction network. INS-related targets derived from peripheral blood mononuclear cells in the Gene Expression Omnibus (GEO) database were intersected with GAD targets to establish a protein-protein interaction (PPI) network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify the key pathways. Experimental validation employed a para-chlorophenylalanine (PCPA)-induced INS rat model, integrating behavioral tests, histopathology, and inflammatory cytokine quantification. Results: Network pharmacology revealed multi-target, multi-pathway actions of GAD against INS, with the TNF signaling pathway identified as a critical axis. Animal experiments demonstrated that GAD significantly improved sleep architecture in INS rats, reduced serum and hippocampal levels of TNF-α and interleukin-1β (IL-1β), and downregulated phosphorylated NF-κB p65 (p-p65) expression, indicating suppression of TNF-driven neuroinflammation. Conclusion: GAD ameliorates INS in a rat model by inhibiting TNF-mediated inflammatory signaling, offering a potential mechanistic basis for its therapeutic use in INS management.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.