Abstract:

Based on network pharmacology and animal experiment, the mechanism of action of Rhei Radix et Rhizoma-Natrii Sulfas (RRR-NS) in the treatment of acute pancreatitis (AP) was studied. Active components and potential targets of the drugs were identified using the TCMSP database. A "drug–chemical component–potential target" network was constructed using Cytoscape 3.7.2, while protein-protein interaction (PPI) networks were established via the STRING database. GO and KEGG enrichment analyses were performed using the DAVID database and R software. Molecular docking was carried out with AutoDock to assess the binding affinity between the active compounds and key targets. Subsequently, an AP mouse model was induced using 50 g/L sodium taurocholate for in vivo validation. Network pharmacology analysis identified 14 active compounds in RRR-NS and 58 potential targets, of which 51 were associated with AP. KEGG pathway enrichment indicated that these targets were primarily involved in pathways related to hepatitis B, tumor protein p53 (TP53), and the mitogen-activated protein kinase (MAPK) signaling pathway. PPI analysis revealed that seven core proteins, including tumor necrosis factor (TNF), interleukin-1β (IL-1β), and TP53, are likely key targets for RRR-NS in the treatment of AP. Animal experiments demonstrated that RRR-NS significantly ameliorated histopathological damage in the pancreas and liver tissues of AP rats, reduced serum levels of α-amylase, lipase, IL-1β, and TNF-α, and decreased the expression of cysteine aspartate protease-3 (Caspase-3),TP53,and jun proto-oncogene (JUN) proteins in pancreatic tissues.In conclusion,RRR-NS may exert therapeutic effects on acute pancreatitis by downregulating the expression of Caspase-3,TP53,and JUN,thereby inhibiting the inflammatory response and mitigating AP.

Key words: Rhei Radix et Rhizoma-Natrii Sulfas drug pair, acute pancreatitis, network pharmacology, molecular docking, inflammation