Ionomics and proteomics analysis of the pancreatic repair in a murine severe acute pancreatitis model treated with Qingyi decoction

Background Current therapeutic options for severe acute pancreatitis (SAP) remain limited. The integration of traditional Chinese and Western medicines offers a promising approach for patients with SAP, with Qingyi decoction (QYD) emerging as a classic and effective formula for this condition. Nevertheless, its precise mechanism—particularly regarding ionomics and proteomics—requires further elucidation. Purpose This study aimed to investigate the possible underlying mechanisms by exploring the characteristics and relationships of alterations in ionomics and proteomics profiles during pancreatic repair in a mouse model of SAP treated with QYD. Methods The therapeutic efficacy of QYD in SAP was validated through pathological section analysis and immunohistochemistry. Total elemental analysis of serum and mouse tissues was performed using inductively coupled plasma–mass spectrometry to identify relevant target elements. XPS analysis was employed to determine the chemical speciation of the target elements. Proteomic analysis, combined with KEGG, GO enrichment and STRING protein–protein interaction analyses, elucidated the protein molecules and biological pathways and the core proteins involved in QYD-mediated SAP treatment were verified by Western blotting. Finally, to clarify the relationship between changes in ion content and alterations in oxidative phosphorylation-related proteins and mitochondria-associated proteins, we conducted Pearson correlation analysis and mitochondrial morphological identification. Results QYD effectively alleviated symptoms of lipopolysaccharide-induced SAP. During this process, metal ions—particularly zinc ions—underwent significant coordination changes. Five core proteins were extracted from the proteomics section, and oxidative phosphorylation emerged as a critical pathway in this therapeutic mechanism. Furthermore, correlation analysis revealed close connections between ionic changes (Zn, Cu, Fe, Ca, Mg, Mn, and Se) and the expression profiles of oxidative phosphorylation-related proteins (Nduf and Atp5f1b) and mitochondrial-associated proteins (Tfam, Ppp3ca, and Myef2), which were also consistent with the observed changes in mitochondrial morphology. Conclusion The therapeutic mechanism of QYD in SAP may involve the ionic spectrum, especially zinc, modulating disease progression through mitochondrial oxidative phosphorylation.