ArticleAnimal models and experimental medicine2026
Citrus aurantium honey-mediated gut homeostasis and anti-inflammation via Thorl/Nprl2-TORC1 signaling: Network pharmacology and Drosophila validation.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Effects of a Combined Antimicrobial Peptide andMicroorganisms · 2026Article
- Citrus aurantium honey-mediated gut homeostasis and anti-inflammation via Thorl/Nprl2-TORC1 signaling: Network pharmacology and Drosophila validation.Animal models and experimental medicine · 2026Article
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7 authors.
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Abstract
backgroundThis study aimed to investigate the mechanisms by which Citrus aurantium honey modulates gastrointestinal motility, inflammation, and barrier function using network pharmacology and Drosophila melanogaster models.
methodsUltra-high-performance liquid chromatography coupled with Q Exactive high-field mass spectrometry (UHPLC-Q Exactive HF-MS) characterized the chemical profile. Network pharmacology predicted targets and enriched pathways, and molecular docking validated core component-target binding. In lipopolysaccharide (LPS)-induced Drosophila intestinal injury models, functional assays (fecal excretion, intestinal transit, barrier integrity) and mechanistic analyses (reactive oxygen species [ROS] levels, TORC1 pathway-related protein/gene expression) were performed.
resultsNetwork pharmacology revealed 17 key targets enriched in calcium signaling, cAMP/cGMP-PKG, and neuroactive ligand-receptor pathways. In Drosophila, honey dose-dependently (0.25% < 0.5% < 1%) enhanced intestinal motility (increased volume of stool and shorter transit time) and reduced inflammation (reduced ROS levels and improved barrier integrity, p < 0.01). Mechanistically, honey inhibited TORC1 overactivation by reducing 4E-BP phosphorylation and regulating Thor/Nprl2 expression.
conclusionsC. aurantium honey exerts gastrointestinal effects via a "multi-component, multi-target" mechanism. It modulates smooth muscle contraction through calcium/cAMP/cGMP pathways and alleviates inflammation by suppressing TORC1 signaling, highlighting its potential as a dietary intervention for dysmotility and inflammation.
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