ArticleFrontiers in pharmacology2026
Molecular and metabolic mechanisms of quercetin in liver fibrosis: an integrated network pharmacology, metabolomics, and molecular dynamics study.
Article in Frontiers in pharmacology, 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
Introduction: Liver fibrosis, a severe chronic liver injury sequela, lacks effective therapies. Quercetin, a natural flavonoid, exhibits multi-target anti-fibrotic potential. Methods: This study integrated network pharmacology,metabolomics, molecular docking, and molecular dynamics simulations to investigate its mechanisms. Results: Network analysis identified 203 overlapping targets, with core targets including protein kinase B (AKT1), interleukin-6 (IL6), tumor protein p53 (TP53), and tumor necrosis factor (TNF), which were enriched in PI3K-Akt and TNF signaling pathways. In CCl4- induced rats (quercetin 50 mg/kg/day), quercetin alleviated pathological damage, significantly reduced collagen area by 43.1% (P = 0.006), and lowered serum alanine aminotransferase, aspartate aminotransferase, and type III procollagen levels. Metabolomics revealed 32 differential metabolites, implicating multiple metabolic pathways including lipid and amino acid metabolism. Molecular docking showed strong binding to AKT1 (5.8 kcal/mol) and TNF (7.2 kcal/ mol), with stable complexes over 100 ns simulations. QPCR was used to detect the expression of PI3K/AKT1 core targets in liver tissue, and experimental verification confirmed the predicted key targets. Conclusion: This multi-faceted study elucidates quercetin's anti-fibrotic mechanism, laying a foundation for its therapeutic development.
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