ArticleCellular and molecular life sciences : CMLS2025
Quercetin alleviates acute pancreatitis by modulating glycolysis and mitochondrial function via PFKFB3 inhibition.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Beyond Supportive Care: Mitochondria as a Strategic Therapeutic Avenue in Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- Regulating Glucose Metabolism Enzymes for Osteoporosis Therapy: Current and Future Approaches.International journal of molecular sciences · 2026Review
- Macrophage Membrane-Cloaked, ROS-Triggered Quercetin Nanocarriers Target Ovarian Lesions to Treat Polycystic Ovary Syndrome.Advanced healthcare materials · 2026Article
- Translational Pharmaco-Nutritional Approaches in the Management of Clinical Acute Pancreatitis-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectiveAcute pancreatitis (AP) is a severe inflammatory disease associated with dysregulated glycolysis and mitochondrial dysfunction. This study investigates the therapeutic potential of quercetin, a novel PFKFB3 inhibitor, in modulating glycolysis and mitochondrial function to alleviate AP.
methodsWe conducted homology analysis of the PFKFB3 protein and identified quercetin as a potential inhibitor through molecular docking. In vitro experiments using a cerulein-induced inflammatory pancreatic cell model assessed the effects of quercetin on PFKFB3 expression, glycolysis, and mitochondrial function. In vivo validation was performed using an AP rat model to evaluate the impact on inflammation, tissue damage, and metabolic status.
resultsQuercetin significantly reduced PFKFB3 expression, inhibited glycolysis, and improved mitochondrial function in inflammatory pancreatic cells. In the AP rat model, quercetin treatment decreased serum amylase and lipase levels, reduced inflammatory markers (TNF-α and IL-6), and alleviated pancreatic tissue damage, as evidenced by histological analysis.
conclusionQuercetin effectively modulates glycolysis and mitochondrial function by inhibiting PFKFB3, thereby reducing inflammation and tissue damage in AP. These findings highlight the potential of quercetin as a novel therapeutic agent for AP.
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Registered trials
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