An Nrf-2 mediated mechanism for LXA4 protection on E-cadherin in airway epithelium is proposed.
Fluorescence resonance energy transfer analysis indicted that LXA4 promoted the dissociation of Nrf2 and its negative regulator, Keap1.
LXA4 could regulate the mitochondrial redox status in LPS-treated mice from a higher oxidative state to a more reduced state.