Efficacy of Tounongsan decoction on pyogenic liver abscess: network pharmacology and clinical trial validation.

OBJECTIVE: To elucidate the molecular mechanisms governing the effect of Tounongsan decoction (, TNS) on the pyogenic liver abscess.

METHODS: Based on oral bioavailability and drug-likeness, the main active components of TNS were screened using the Traditional Chinese Medicine Systems Pharmacology platform. The GeneCard and UniProt databases were used to establish a database of pyogenic liver abscess targets. The interactive network map of drug-ingredients-target-disease was constructed using Cytoscape software (Version 3.7.2). A protein-protein interaction network was constructed using the STRING database, and the related protein interaction relationships were analyzed. biological process of gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed for the core targets. Finally, a clinical trial was performed to verify the reliability of the network pharmacology.

RESULTS: Forty active components of TNS decoction were obtained, and 61 potential targets and 11 proteins were identified. Pathways involved in the treatment of pyogenic liver abscess include the phosphatidylinositide 3-kinases-protein kinase B (PI3K-AKT), advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE), and tumor necrosis factor (TNF) signaling pathways. The results of network pharmacology analysis combined with clinical trials validated that TNS decoction could alleviate the inflammatory response of pyogenic liver abscesses by decreasing interleukin 6 (IL-6) levels.

CONCLUSIONS: TNS decoction has the characteristics of being multi-system, multi-component, and multi-target. Active ingredients in TNS, such as quercetin, kaempferol, fisetin, and β-sitosterol, have strong potential to be candidate drugs for treating pyogenic liver abscesses. The possible mechanism of TSN decoction includes regulating immune and inflammatory responses and reducing IL-6 production to control inflammatory development.