In this study, we found that emodin to a great extent downregulated the levels of IL-1β, IL-18, TNF-α, and MPO activity in lung tissue in both two types of SAP-ALI models, which is consistent with the protective role of emodin in reducing oxidative stress and inflammasome signals (Xia et al., 2019). Here, IL18 is linked to acute respiratory distress syndrome.