MECHANISM OF QINGYI DECOCTION AGAINST ACUTE PANCREATITIS: A NETWORK PHARMACOLOGY ANALYSIS

Yi Wu^{1, 3, 4}, Xiao-long Tang^{3, 4}, Jing-Dong Li^{1, 2, 4, *}

¹Jinan University, No.601 Huangpu Avenue West, Guangzhou, 510632, China - ²Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, China - ³Department of Gastrointestinal Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, China - ⁴Institute of Hepato-Biliary-Pancreatic-Intestinal disease, North Sichuan Medical College, Nanchong 637000, China

Background: Qingyi decotion (QLD) is a commonly used herbal for alleviating acute pancreatitis (AP) in China. whereas the crucial compounds and their functional targets remain elusive. 

Methods: We employed the TCMSP database to find the main active compounds of QYD and their prediction of targets. The DisGeNET, OMIM, PharmGKB, and NCBI database were enrolled to search for pathogenetic AP-related targets. Through the Cytoscape, the interaction network of QYD and AP targets was created to illuminate the relationship between the compounds of QYD and AP. Based on the PPI network, the core targets were filtrated. GO and KEGG enrichment analysis illustrated the molecular function of QYD in the treatment of AP. Molecular docking further certified the credibility of the relationship between compounds of QYD and targets of AP. 

Results: 97 AP-related active compounds were found, and 65 potential targets for AP were identified. Quercetin, kaempferol, wogonin, baicalein, and isorhamnetin are the top 5 useful compounds of QYD in the treatment of AP. Through the PPI network, 15 core targets of QYD in the treatment of AP were screened out. The biological functions and processes (BP) include response to lipopolysaccharide, response to molecule of bacterial origin, response to nutrient levels, cellular response to chemical stress. Pathways contain the AGE−RAGE signaling pathway in diabetic complications, Fluid shear stress and atherosclerosis, TNF signaling pathway, IL−17 signaling pathway and HIF−1 signaling pathway. Molecular docking indicated that the compounds of QYD have an excellent affinity to the targets of AP. 

Conclusion: QYD has the characteristics of “multiple-drugs, multiple-targes” in the treatment of AP. Quercetin, kaempferol, wogonin, baicalein, and isorhamnetin may be the candidate drugs for the treatment of AP. This finding may further contribute to novel drug development.