Angelicin attenuates sepsis-associated acute liver injury via p38 MAPK inhibition and NF-κB-mediated Nrf2/Keap1 activation to suppress inflammation and oxidative stress

• Angelicin significantly alleviates sepsis-associated acute liver injury (SALI) by improving liver function and reducing pathological damage in a CLP-induced mouse model. • ANG suppresses inflammation by downregulating pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and upregulating anti-inflammatory IL-10, via inhibition of NF-κB and p38 MAPK pathways. • ANG exerts antioxidant effects by reducing MDA and ROS levels while increasing GSH, CAT, and SOD activities, through activation of the Nrf2/Keap1 pathway. • Mechanistically, ANG-induced Nrf2/Keap1 activation is dependent on NF-κB inhibition, highlighting a novel crosstalk and positioning ANG as a promising therapeutic candidate for SALI.