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Objective <p>Acute 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.</p> Methods <p>We conducted homology analysis of the PFKFB3 protein and identified quercetin as a potential inhibitor through molecular docking. <i>In vitro</i> experiments using a cerulein-induced inflammatory pancreatic cell model assessed the effects of quercetin on PFKFB3 expression, glycolysis, and mitochondrial function. <i>In vivo</i> validation was performed using an AP rat model to evaluate the impact on inflammation, tissue damage, and metabolic status.</p> Results <p>Quercetin 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.</p> Conclusion <p>Quercetin 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.</p>

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Quercetin alleviates acute pancreatitis by modulating glycolysis and mitochondrial function via PFKFB3 inhibition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月13日

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  • Hai Jiang,
  • Jia Liu,
  • Zhipeng Xu,
  • Qi Song,
  • Junjie Tao,
  • Heng Zhu,
  • Qiliang Li,
  • Lei Li

摘要

Objective

Acute 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.

Methods

We 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.

Results

Quercetin 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.

Conclusion

Quercetin 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.