Elucidating the anti-fibrotic mechanisms of Abrus cantoniensis in hepatic fibrosis using network pharmacology and proteomics.

This study aimed to elucidate the effects and underlying mechanisms of Abrus cantoniensis in treating mice hepatic fibrosis, thereby providing a rationale for its clinical application. To investigate A. cantoniensis effects in hepatic fibrosis, we established a carbon tetrachloride-induced mouse model validated by histopathology. Potential active compounds were revealed through LC-MS, and core targets were identified by network pharmacology integrated with proteomics. Validation was performed using molecular docking, molecular dynamics, and immunohistochemistry. Histopathology confirmed the anti-hepatic fibrosis effects of A. cantoniensis. The LC-MS analysis identified 420 compounds, while network pharmacology and proteomics revealed 208 and 738 key targets, respectively. Functional enrichment revealed that these targets were involved in hepatic fibrosis-related processes. Intersecting both analyses identified four core targets: BRAF, CDK2, DNMT1, and PDGFRB. Molecular docking and dynamics simulations demonstrated strong and stable binding between the potential active compounds and these targets, which was further validated by immunohistochemistry showing suppressed expression of the targets. Our integrated multi-omics study elucidated that the anti-hepatic fibrosis effect of A. cantoniensis was mediated by the core targets BRAF, CDK2, DNMT1, and PDGFRB, thus supporting its development as a standardized phytomedicine.