In our study, we found that H-SN1 treatment attenuated the inflammatory response in LPS-induced ALI, and its protective effect might involve the inhibition of the production of inflammatory mediators such as TNF-α, IL-6, and IL-1β, partially by interfering with the ERK1/2 and NF-κB signaling pathways. The gene discussed is IL6; the disease is acute respiratory distress syndrome.