Accordingly, in this study, to elucidate the role of SIN in ALI and the possible link between SIN and A2AR in ALI, we constructed a LPS-induced ALI model in both wild type (WT) and A2AR gene knockout (KO) mice, and investigated the effect of SIN on lung water content, the PaO2/FIO2 (P/F) ratio, histological signs of pulmonary injury, neutrophil infiltration and expression of the inflammatory cytokines TNF-α and IL-1β. This evidence concerns the gene ADORA2A and acute respiratory distress syndrome.