To study the effect of Lyn kinase on the mice with chronic obstructive pulmonary disease (COPD) and its possible mechanism.

C57BL/6j wild type mice and C57BL/6j Lyn⁺ transgenic mice were randomly divided into a wild type control group (WT group, n=8), a wild type model group (WT+ COPD group, n=8), a Lyn⁺ control group (Lyn+ group, n=8), and a Lyn+ model group (Lyn⁺ + COPD group, n=8). The mice in the WT+ COPD group and the Lyn⁺ + COPD group were modeled by COPD using cigarette smoking and lipopolysaccharide injection into the airway. And 60 days later, the related lung function indicators were recorded by a lung function tester, the pathological changes in the lung tissues were observed with HE staining, the contents of IL-1β, IL-6, IL-10 and TNF-α in the serum and in the alveolar lavage fluid (BALF) were detected with ELISA method, and the expression of Erk-sp1 signaling pathway-related proteins in the lung tissues was detected with Western blotting method.

The lung tissues of the mice in the WT group and in the Lyn+ group had no obvious pathological changes. The alveolar structure in the lung tissues of the WT+ COPD group was damaged, and a large number of inflammatory cell infiltration occurred. The pulmonary alveolar rupture and inflammatory cell infiltration in the Lyn⁺ + COPD group were improved compared with that of the WT+ COPD group. In the WT+ COPD group, Ri increased, Cdyn and FEV 0.3%/FVC decreased, the contents of IL-1β, IL-6, IL-10 and TNF-α in the serum and BALF were all increased, pErk, Erk and sp1 protein levels in the lung tissues increased compared with the WT group, and the differences were statistically significant between the two groups (P<0.05). In the Lyn⁺ + COPD group, Ri was increased while Cdyn and FEV0.3%/FVC were decreased, and the levels of IL-1β, IL-6, IL-10 and TNF-α in the serum and BALF were increased, the protein levels of pErk, Erk and sp1 increased in the tissues compared with the Lyn+ group, and the differences were statistically significant between the two groups (P<0.05). In the Lyn⁺ + COPD group, Ri decreased while Cdyn and FEV0.3%/FVC increased, the contents of IL-1β, IL-6, IL-10 and TNF-α decreased, the protein levels of pErk, Erk and sp1 decreased compared with the WT+ COPD group, and the differences were statistically significant between the two groups (P<0.05).

Lyn kinase can alleviate COPD in mice by inhibiting the inflammatory response, and its mechanism may be closely related to Erk-sp1 signaling pathway.