Integrating serum pharmacochemistry, network pharmacology and metabolomics analysis to explore the possible mechanism of Qingjiehuagong decoction in the treatment of acute pancreatitis

Background: The Qingjiehuagong decoction (QJHGD), which has been used in clinical trials to treat acute pancreatitis (AP), has demonstrated encouraging results. Methods: In this particular investigation, we used both metabolomics and network pharmacology to investigate the fundamental processes and targets that QJHGFD employs to cure AP. Results: Using a cerulein-induced rat model of AP, we showed that QJHGD effectively improved pancreatic tissue damage and reduced serum levels of AMY, LPS, IL-1 & beta;, IL-6, IL-8 and TNF-& alpha;. In total, 28 blood entry compounds derived from QJHGD were identified by ultra-performance liquid chromatography-high resolution mass spectrometry technology. The intersecting target genes of 108 genes associated with identified compounds in QJHGD and AP disease genes were identified using a network pharmacology approach. The protein interaction network revealed AKT1, TNF-& alpha;, IL-6, VEGFA, and TP53 as important targets. Gene ontology analysis showed that response to stimulus, molecular function regulator and organelle part were the main functions, and Kyoto Encyclopedia of Genes and Genomes analysis showed that 20 pathways such as AGE-RAGE signaling pathway in diabetic complications and the IL-17 signaling pathway were the main pathways involved in the anti-AP effects of QJHGD. Thirty-two potential metabolic markers and 13 possible metabolic pathways were identified by metabolomics analysis. Combined network pharmacological analysis revealed that QJHGD affects four metabolic pathways (tryptophan metabolism; glycolysis and gluconeogenesis metabolism; valine, leucine and isoleucine degradation metabolism; the urea cycle and metabolism of arginine, proline, glutamate, aspartate and asparagine), five metabolites (indole-3-acetate, pyruvate, methylmalonate, L-citrulline, N-acetyl-l-glutamate) and four related targets (AKT1, ALDH2, NOS2, NOS3) to combat inflammation. The strong affinity of QJHGD's interactions with its primary targets was established by molecular docking and molecular dynamics simulations. Conclusion: This research investigate the critical targets and mechanisms of QJHGFD for treating AP. The results of this investigation provide novel tactics and complementary techniques for the clinical treatment of AP.