This study was to investigate antioxidant activities of the ethanol extract from young edible leaves of Ficus vasculosa in vitro and in vivo. Ficus vasculosa ethanol extract (FVEE) showed significantly higher reducing power and α,α-diphenyl-β-picrylhydrazyl (DPPH) radical scavenge activity than vitamin C (P < 0.05). FVEE also showed an activity to resist the D-galactose-induced aging in mice assessed by serum and tissue levels of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). Total serum and tissue oxidative status, total antioxidantresponse, glutathione (GSH) and malondialdehyde (MDA) levels have been also measured. Pretreatment with FVEE at 200 mg/kg·body weight significantly increased enzyme activity of SOD and CAT in serum and hepatic tissue (P < 0.05), as well as significantly increased enzyme activity of SOD in kidney (P < 0.05). Furthermore, high concentration of FVEE pretreatment significantly increased the level of GSH in serum, hepatic tissue and kidney (P < 0.05), meanwhile significantly decreased MDA production in hepatic tissue and kidney (P < 0.05). In addition, the phytochemical investigation discovered six previously described compounds from FVEE, naringenin (1), vanillic acid (2), 9, 16-dioxo-10, 12, 14-octadeca-trienoic acid (3), 2, 6-dimethoxy-1, 4-benzoquinone (4), apigenin (5) and norartocarpetin (6), and all compounds were isolated from this plant for the first time. Among the various compounds found, the rare highly unsaturated fatty acid 9, 16-dioxo-10, 12, 14-octadeca-trienoic acid (3) has been identified, which had been isolated only once before from F. vasculosa. Evaluation of the antioxidant activity of isolated compounds showed naringenin (1) to be the most active. According to our research, FVEE present very high antioxidant activity in vitro due to the presence of several compounds known for their antioxidant activity such as flavonoid and phenolic acid. In vivo, the ethanol extract had improvement effects against D-galactose-induced aging by reducing oxidative stress.

Vanillic acid (VA) is a natural phenolic acid compound that is widely found in various foods and medicinal plants, with a remarkable antifibrotic effect observed in animal studies, but its exact antifibrotic mechanism remains unclear. Herein, hepatic function, fibrotic index, and histopathological, microbiome, and metabolomic methods were used to investigate the potential mechanisms behind the improvement effect of vanillic acid against thioacetamide (TAA)-induced liver fibrosis in mice. Our results showed that VA reversed TAA-induced liver fibrosis manifested a decrease in collagen fiber deposition, serum transaminase, serum hepatic fibrotic index, and liver inflammation indicator levels. When analyzed, TAA injection mainly increased the abundance of Akkermansia and Roseburia and significantly reduced the abundance of Anaerotruncus. VA reversed these changes back to normal levels to varying degrees. Metabolomic profiling demonstrated that VA treatment was efficacious in modulating several key liver metabolites involved in neuroactive ligand–receptor interaction, prolactin signaling pathway, estrogen signaling pathway, and glutathione metabolism. Conclusively, VA may ameliorate liver damage and suppress the fibrogenesis caused by thioacetamide by correcting intestinal microbiota disorders and promoting normal hepatic metabolism. This research provides a novel perspective on vanillic acid as a dietary supplement for hepatic fibrosis improvement.