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

This study performed to study the change of oncostatin M(OSM) and its downstream signalingpathways in gefitinib-relieved pulmonary fibrosis in mice. KM female mice(n=36) were randomly divided into 3groups: the mice in control group were administered with saline aerosol intratracheally, the mice in fibrosis groupwere administered with bleomycin at a dose of 3 mg/kg aerosol intratracheally, while the mice in gefitinib group wereadministered with bleomycin at a dose of 3 mg/kg aerosol intratracheally and then were gastrically perfused withgefitinib at a dose of 20 mg/kg. All mice were sacrificed at 14 d after the treatment and the lungs were collected forhematoxylin eosin and Masson’s trichrome staining to exam pathological change. The expression of OSM and α-SMAat m RNA 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, collagenaccumulation, the m RNA 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 underlyingmechanism may be involved in inhibiting the expression of OSM and downstream signaling pathways.