Effect of FA on LPS-induced cellular inflammation, oxidative stress and apoptosis. Through the canonical NF-κB pathway, TLR4 recognizes extracellular LPS and transduces signals via MyD88 to activate NF-κB-mediated proinflammatory gene transcription. In addition, ligated TLR4 promotes the interaction between Park7 and P47phox, which increases NOX-mediated ROS generation. Subsequently, excessive ROS accumulation in the cytoplasm leads to a loss of the MMP, mitochondria-dependent apoptosis and uncoupling of Nrf2-Keap1 and IκBα-NF-κB. Most notably, although dissociated Nrf2 is responsible for anti-inflammatory and antioxidant activity, its levels were increased after 12 h of LPS treatment but did not block the inflammation and oxidative stress induced by NF-κB in the early stage. However, FA interference advances the activation of Nrf2, consequently relieving the inflammatory response and oxidative stress to inhibit cellular apoptosis and promote BMEC survival.