Gefitinib downregulates the expression of OSM and inhibits bleomycin-induced pulmonary fibrosis

ZHENG Linxin; MAI Yumei; DU Haijian; LI Li; LI Weifeng

doi:10.13431/j.cnki.immunol.j.20160060

Abstract：This study performed to study the change of oncostatin M (OSM) and its downstream signaling pathways in gefitinib-relieved pulmonary fibrosis in mice.KM female mice (n=36) were randomly divided into 3 groups:the mice in control group were administered with saline aerosol intratracheally,the mice in fibrosis group were administered with bleomycin at a dose of 3 mg/kg aerosol intratracheally,while the mice in gefitinib group were administered with bleomycin at a dose of 3 mg/kg aerosol intratracheally and then were gastrically perfused with gefitinib at a dose of 20 mg/kg.All mice were sacrificed at 14 d after the treatment and the lungs were collected for hematoxylin eosin and Masson' s trichrome staining to exam pathological change.The expression of OSM and α-SMA at mRNA and protein level were determined by RT-PCR and Western blotting;the protein levels of ERK1/2,P-ERK1/2,P38,and P-P38 were detected by Western blotting.Data showed that the pathological injury,collagen accumulation,the mRNA expression of OSM and α-SMA,the protein levels of OSM,α-SMA,p-ERK1/2/ERK1/2,p-P38/P38 in the lung tissues in bleomycin group was significantly increased compared with that in control group,and the above-mentioned index in gefitinib group was significantly relieved compared with that in bleomycin group.Taken together,Gefitinib significantly relieves bleomycin-induced pulmonary fibrosis in mice.The underlying mechanism may be involved in inhibiting the expression of OSM and downstream signaling pathways.