In summary, luteolin can exert ameliorative effects on LPS-induced ALI through various pathways, such as acting as an anti-inflammatory drug (that inhibits the activity of Hsp90, reduces IL-10 levels, and inhibits NF-κB and MAPK pathways) and an antioxidant (that eliminates excess ROS and enhances antioxidant enzyme activity), as well as improving the function of the pulmonary alveolar ENaC (that activates alveolar ENaC and regulates JAK/STAT pathway) in LPS-induced ALI. This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.