OBJECTIVE To explore the anti-liver fibrosis mechanism of wine-processed Polygonati Rhizoma.

METHODS The chemical constituents of wine-processed Polygonati Rhizoma were detected and analyzed using liquid chromatography-mass spectrometry(LC-MS). Meanwhile, network pharmacology was adopted to predict potential biological targets and signaling pathways. Molecular docking was performed to validate the binding interactions between the screened active components and key targets of liver fibrosis. A rat model of liver fibrosis was induced by carbon tetrachloride(CCl₄), and the anti-liver effects of wine-processed Polygonati Rhizoma were evaluated through liver phenotypic analysis, histopathological examination, and serum biochemical analysis. Western blotting was further used to verify the pathways predicted by network pharmacology.

RESULTS A total of 28 chemical constituents were identified. Network pharmacology screening revealed 17 active components and 235 intersection targets. The PI3K/Akt signaling pathway might serve as one of the major pathways underlying the anti liver fibrosis effect of wine-processed Polygonati Rhizoma. Animal experiments demonstrated that wine-processed Polygonati Rhizoma could alleviate CCl₄-induced liver fibrosis and exert anti-liver effects by inhibiting the PI3K/Akt signaling pathway.

CONCLUSION Wine-processed Polygonati Rhizoma exerts a protective effect against CCl₄-induced liver fibrosis through multiple components, multiple targets, and multiple pathways, and its protective mechanism may be associated with the inhibition of the PI3K/Akt signaling pathway.