Given that CSF effectively reduced the production of pro‐inflammatory cytokines and chemokines in lung tissues of mice with LPS‐induced ALI, and that LPS‐stimulated classical NF‐κB signaling is a key driver of ALI pathogenesis and progression (Quinton and Mizgerd 2011; Quinton et al. 2018), this study further investigated whether CSF could block the TLR4/MyD88/NF‐κB p65 signaling pathway using immunoblotting, immunofluorescence, and qPCR. This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.