OBJECTIVE： To study the improvement effect and mechanism of Meng medicine Wuwei Shaji powder （WSP） on smoke-induced lung inflammation injury in mice. METHODS： ICR mice were randomly divided into blank group （normal saline）， model group （normal saline） and WSP group （2 g/kg）. Mice in model group and WSP group received passive smoking to induce model of lung inflammation injury， and intragastrically administrated relevant medicine when modeling， once a day， for 28 d. After administration， enzyme-linked immunosorbent assay was used to detect the tumor necrosis factor α （TNF-α）， interleukin-1β （IL-1β）， IL-6， IL-10 levels in bronchoalveolar lavage fluids （BALF）； the pathological changes of lung tissue were observed by optical microscope after hematoxylin-eosin staining； Western blot was adopted to detect the protein expressions of extracellular signal-regulated kinase （ERK1/2）， phosphorylated ERK1/2 （p-ERK1/2）， p38 mitogen-activated protein kinase （p38 MAPK）， phosphorylated p38 MAPK （p-p38 MAPK）， nuclear factor kappaB p65 （NF-κB p65） and phosphorylated NF-κB p65 （p-NF-κB p65） in lung tissue of mice. RESULTS： Compared with blank group， TNF-α， IL-1β， IL-6 levels in BALF in model group were obviously increased （P＜0.01）； lung tissue showed significant inflammatory lesions； and the protein expressions of p-ERK1/2， p-p38 MAPK， p-NF-κB p65 in lung tissue were obviously increased （P＜0.01）. Compared with model group， TNF-α， IL-1β levels in BALF in WSP group were obviously decreased （P＜0.05）； inflammation injury in lung tissue was obviously improved； and protein expressions of p-p38 MAPK and p-NF-κB p65 in lung tissue were obviously decreased （P＜0.05）. CONCLUSIONS： WSP shows improvement effect on smoke-induced lung inflammation injury in mice， which might be by blocking the p38 MAPK， NF-κB p65 phosphorycation to inhibit the high expression of inflammatory factors as TNF-α and IL-6.