Additionally, molecular docking indicated that BKA directly blocks the binding site of Nrf2 with Keap1.<h4>Conclusions</h4>BKA reduces APAP-induced acute liver damage by inhibiting oxidative stress by activating the Keap1/Nrf2/HO-1 signaling pathway, providing a theoretical basis for BKA as a potential therapeutic agent for APAP-induced liver injury. The gene discussed is KEAP1; the disease is injury.