ArticleAmerican journal of translational research2026
Network pharmacology identifies the mechanisms of action of Jianpi Yanggan Pill in treating diarrhea-predominant irritable bowel syndrome.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate the molecular mechanisms of Jianpi Yanggan Pill (JPYGP) in treating Diarrhea-predominant irritable bowel syndrome (IBS-D) using an integrated network pharmacology approach combined with experimental validation.
methodsThe chemical constituents of JPYGP were identified by ultra-high performance liquid chromatography-high-resolution mass spectrometry (UHPLC-MS/MS), and bioactive compounds were screened using various databases. Candidate targets was predicted, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment studies. An IBS-D rat model was established using acetic acid enema combined with restraint stress. The therapeutic potential of JPYGP was further validated through biochemical assays, including Western blotting and enzyme-linked immunosorbent assay (ELISA), to assess the involvement of the C-X-C motif chemokine ligand 8 and extracellular signal-regulated kinase (CXCL8-ERK) signaling pathway.
resultsUHPLC-MS/MS analysis identified 2,309 candidate compounds in JPYGP, among which 20 were bioactive. A total of 660 targets were predicted, of which 414 overlapped with IBS-D-related targets. Enrichment analysis highlighted that these targets were mainly involved in inflammatory and MAPK pathways. In a living organism, JPYGP noticeably alleviated diarrhea symptoms and visceral pain, reduced colonic tissue damage, inhibited mast cell activation, and downregulated the expression of CXCL8 and phosphorylated ERK1/2.
conclusionJPYGP exerts therapeutic effects on IBS-D via a multi-component, multi-target mechanism, primarily by suppressing the CXCL8-ERK pathway, thereby attenuating colonic inflammation and visceral hypersensitivity.
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