In the present study, we reported that HA1600 prevented smoke-induced ALI and downregulation of MALAT1, and the overexpression of MALAT1 by adenovirus in the lung exhibited protective effects against smoke-induced ALI and upregulated the protein level of SOCS-1, providing a novel insight into the therapeutic application and mechanism of action of HA1600. This evidence concerns the gene MALAT1 and acute respiratory distress syndrome.