Objective To investigate the effects and mechanisms of Mongolian medicine Eligen Tang (ET) in the treatment of hepatic fibrosis, employing non-targeted metabolomics and experimental validation.Methods Fifty male SD rats were randomly assigned to five groups: control group, model group, and low, medium, and high-dose ET groups (90 mg/100 g, 180 mg/100 g, 450 mg/100 g). A liver fibrosis model was induced by intraperitoneal injection of carbon tetrachloride (CCl?), and after 21 days of ET treatment, liver tissues were collected for non-targeted metabolomics analysis. Pathological changes were assessed using hematoxylin-eosin (HE) staining. Masson's trichrome staining was used to evaluate liver fibrosis. Enzyme-linked immunosorbent assay (ELISA) measured serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and hydroxyproline (Hyp). Real-time quantitative PCR was used to quantify mRNA levels of α-smooth muscle actin (α-SMA) and collagen I. Western blotting was employed to detect the expression of α-SMA, collagen I, peroxisome proliferator-activated receptor (PPAR) signaling proteins, and proteins involved in the transforming growth factor-β (TGF-β) signaling pathway in liver tissues.Results Compared with the control group, 83 differential metabolites were identified in the model group (P < 0.05), interstitial fibrosis injury in liver, serum ALT and AST levels, liver Collagen I, α-SMA and Hyp levels, p-Smad2 and p-Smad3 were increased (P < 0.05), and PPAR γ levels decreased (P < 0.05). Compared with the model group, the ET administration group screened 34 different metabolites (P < 0.05), reduced liver fibrosis damage, serum ALT and AST levels, liver Collagen I, α-SMA and Hyp levels, p-Smad2 and p-Smad3 were decreased (P < 0.05), PPAR γ levels increased (P < 0.05), and the effect was better in the ET-H group.Conclusions ET alleviates CCl?-induced hepatic fibrosis in rats by regulating the PPAR and TGF-β.