Therapeutic efficacy and multitarget mechanisms of traditional Chinese medicine in hereditary liver diseases: Insights into bioactive components

Figure 6 Modulation of glucose metabolism, lipid metabolism, and mitochondrial function by traditional Chinese medicine bioactive components. This schematic illustrates the multitargeted metabolic regulatory mechanisms of traditional Chinese medicine-derived compounds across three interconnected pathways: Glucose metabolism, lipid metabolism, and mitochondrial energy homeostasis, highlighting their potential in managing metabolic disorders and liver diseases. Berberine, Astragalus polysaccharide, and Ginsenoside Rg1 activate activated protein kinase (AMPK) signaling, enhancing glucose uptake and glycogen synthesis. Quercetin suppresses gluconeogenesis via the LKB1-AMPK and phosphatidylinositol 3-kinase-protein kinase B-forkhead box protein O1 pathways, reducing hepatic glucose output. Curcumin and baicalin inhibit SREBP-1c-driven fatty acid synthesis (via ACC/FAS downregulation); resveratrol activates AMPK to suppress lipogenesis; ursolic acid and oleanolic acid activate peroxisome proliferator-activated receptor α to promote fatty acid β-oxidation; quercetin and saponins regulate lipid metabolism gene networks. Ginsenoside Rg1 and resveratrol enhance mitochondrial membrane potential (ΔΨm), supporting bioenergetics. Quercetin, salvianolic acid B, and Astragalus polysaccharide improve cellular energy metabolism status, likely via mitochondrial quality control and oxidative phosphorylation optimization. AMPK: Activated protein kinase; PI3K: Phosphatidylinositol 3 kinase; Akt: Protein kinase B; FOXO1: Forkhead box protein O1; PPARα: Peroxisome proliferator-activated receptor α.