Administration of RvD1 intravenously prior to LPS exposure significantly abrogated LPS-induced inflammation, as indicated by histologic ALI score, and blunted elevations in BALF neutrophils, TNFα, and IL-6; RvD1 treatment also significantly inhibited LPS-induced IκBα degradation, NF-κB p65 subunit nuclear translocation, and DNA-binding activity of NF-κB. Furthermore, RvD1 increased protein levels of PPARγ in the nucleus of lung tissues. Here, PPARG is linked to acute respiratory distress syndrome.