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

Figure 2 Mechanisms of metal ion homeostasis regulation and oxidative damage antagonism by traditional Chinese medicine bioactive components in hepatolithiasis-inducing liver diseases. A: Iron homeostasis: Excessive iron accumulation exacerbates hepatobiliary injury in hepatolithiasis-inducing liver diseases (e.g., hereditary hemochromatosis). Berberine and salvianolic acid B directly chelate Fe³⁺/Fe²⁺, reducing the labile iron pool and suppressing Fenton reactions. Astragalus polysaccharide activates the p38 mitogen-activated protein kinase pathway, upregulating hepcidin, which degrades the iron exporter ferroportin to limit systemic iron overload; B: Oxidative damage antagonism: Traditional Chinese medicine components mitigate reactive oxygen species-driven biliary epithelial injury through complementary mechanisms: Curcumin, Astragalus polysaccharide, and ursolic acid activate nuclear factor erythroid 2-related factor 2, inducing antioxidant enzymes (superoxide dismutase, catalase) via the antioxidant response element pathway; quercetin and β-carotene directly scavenge free radicals and inhibit lipid peroxidation; baicalin and salvianolic acid B combine direct reactive oxygen species scavenging with iron chelation to block Fenton-mediated hydroxyl radical generation. MAPK: Mitogen-activated protein kinase; Nrf2: Nuclear factor erythroid 2-related factor 2; ARE: Antioxidant response element; SOD: Superoxide dismutase; CAT: Catalase; ROS: Reactive oxygen species.