In vitro and in vivo antioxidative and hepatoprotective activity of aqueous extract of Cortex Dictamni

Figure 8 Summary of the mechanism underlying Cortex Dictamni aqueous extract inhibition of CCl₄-induced live damage. CCl₄ accumulates in hepatic parenchymal cells and is metabolized by cytochrome P450 2E1 (CYP2E1) to produce free radicals, including CCl₃^- and CCl₃O₂^-, which induce oxidative stress and oxidative injury. CDAE suppresses CCl₄ metabolism by reducing CYP2E1 expression and subsequently inhibiting the production of free radicals. In addition, CDAE activates nuclear factor E2-related factor (Nrf2)-mediated antioxidants, including heme oxygenase-1 (HO-1), NAD(P)H quinine oxidoreductase 1 (NQO1), and γ-glutamylcysteine synthetase catalytic subunit (γ-GCSc), which contribute to the scavenging of free radicals. CDAE: Cortex Dictamni aqueous extract; GSH: Glutathione.