Network pharmacology and molecular docking to explore the potential mechanism of Chlorogenic acid in combined septic acute liver injury

Abstract

Objective To investigate the biological activities and mechanisms of chlorogenic acid (CGA) in treating septic acute liver injury (SALI) using network pharmacology, molecular docking, and in vivo studies. Methods Potential targets related to both chlorogenic acid and septic acute liver injury were searched from public databases. Protein-protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. Molecular docking was performed to predict the binding affinity between the active compounds and core targets. Finally, in vitro and in vivo experiments were carried out for further validation. Results A total of 60 common targets were identified between acute septic liver injury and chlorogenic acid, among which 10 shared core targets were screened using Cytoscape. Molecular docking results indicated that these core targets had good binding activity with chlorogenic acid. In the SALI mouse model, chlorogenic acid demonstrated significant protective effects on the liver and anti-inflammatory properties, acting through the TLR4/NF-κB pathway. Conclusion CGA not only improves pathological damage in acute septic liver injury but also exerts its effects potentially through multiple pathways including TLR4.