[Gefitinib inhibits α-smooth muscle actin expression in mice with bleomycin-induced lung fibrosis].
Journal: 2013/May - Nan fang yi ke da xue xue bao = Journal of Southern Medical University
ISSN: 1673-4254
PUBMED: 21177177
Abstract:
OBJECTIVE
To evaluate the effect of epidermal growth factor receptor tyrosine kinase inhibitor, gefitinib, on the expression of α-smooth muscle actin (α-SMA) in mice with lung fibrosis induced by bleomycin.
METHODS
Thirty male BALB/c mice were randomly divided into control, bleomycin, and bleomycin plus gefitinib groups. The mice in the control group were subjected to intratracheal administration of normal saline, those in bleomycin group received bleomycin (3 mg/kg) intratracheally, and those in bleomycin plus gefitinib group received oral gefitinib (20 mg/kg administering) plus intratracheal bleomycin administration. All the mice were sacrificed 14 days after the treatments, and the left lung was examined pathologically with HE staining and Masson staining and also immunohistochemically for assay of the total EGFR, phosphorylated EGFR and α-SMA. The right lungs were sampled for RT-PCR to detect the mRNA levels of α-SMA.
RESULTS
Gefitinib administration lessened lung fibrosis induced by bleomycin and significantly reduced lung collagen accumulation. The phosphorylation of EGFR in the pulmonary mesenchymal cells and epithelial cells and the expression levels of α-SMA mRNA and protein were inhibited by gefitinib treatment in mice with intratracheal administration of bleomycin (P<0.05).
CONCLUSIONS
Gefitinib offers protection against lung fibrosis induced by bleomycin in mice probably by inhibiting the downstream signals of EGFR and by downregulating the expression of α-SMA.
Relations:
Citations
(1)
Diseases
(1)
Drugs
(4)
Chemicals
(3)
Genes
(2)
Organisms
(3)
Anatomy
(1)
Similar articles
Articles by the same authors
Discussion board
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.