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Multi-omics and preclinical study demonstrates Tiaoqi Daozhi Decoction relieves IBS-C in a rat model, indicating therapeutic action through VIP-PKA-AQP3 axis activation and immune-neural remodeling.
Background/objective This study investigates the molecular mechanisms of Tiaoqi Daozhi Decoction (TQD) in treating irritable bowel syndrome with constipation (IBS-C), focusing on its regulation of the immune-neuro-epithelial network and the VIP–PKA–AQP3 signaling axis. Methods Active components of TQD and potential targets were screened via TCMSP and SwissTargetPrediction. Identification of IBS-C DEGs from GSE146853 dataset constituted our initial step. Candidate therapeutic targets were analyzed through functional enrichment and protein–protein interaction networks. Machine learning models were applied to identify key disease-related biomarkers, followed by molecular docking and molecular dynamics simulations to evaluate compound–target interactions. The therapeutic efficacy of TQD and changes in colonic VIP–PKA–AQP3 signaling-related molecules were further evaluated in a liver-depression syndrome IBS-C rat model. Results Network pharmacology afforded identification of 74 bioactive constituents and 23 coincident putative targets, alongside substantial overrepresentation in inflammatory responses, neurotransmitter modulation, and neuroactive ligand-receptor coupling. Machine learning defined CETP , SELP , and BTK as core signature genes with high diagnostic performance (AUC = 0.714–0.829), with SELP contributing most to the model. Molecular docking and MD simulations confirmed that isodalbergin stable-binds to CETP and hyndarin to BTK. In the liver-depression syndrome IBS-C rat model, TQD significantly improved depressive-like behaviors and intestinal motility dysfunction, with increased colonic expression of VIP, p-PKA/PKA ratio, and AQP3, suggesting involvement of the VIP–PKA–AQP3 signaling pathway. Conclusion TQD alleviates IBS-C by modulating the immune–neuro–epithelial network, with associated changes in the VIP–PKA–AQP3 signaling pathway that may contribute to improvements in intestinal motility dysfunction and epithelial water transport abnormalities.
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Huang et al. (2026) studied this question.
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