Cell Biochemistry and Biophysics

, Volume 70, Issue 1, pp 251–257 | Cite as

Expression and Mechanism of BRP-39 in Bleomycin-Induced Pulmonary Fibrosis in Rat

Original Paper
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Abstract

The purpose of the study was to explore the effects of breast regression protein 39 (BRP-39) in bleomycin-induced pulmonary fibrosis and its mechanism in pulmonary fibrosis by studying change in BRP-39 to provide a novel direction for the treatment of idiopathic pulmonary fibrosis. SPF grade male C57BL/6 rats were randomly divided into three groups, including bleomycin group, bleomycin+ BRP-39 recombinant protein group and control group. HE and Masson staining were applied to test the change in lung tissue after being treated by BRP-39, ELISA was applied to test the expression of TGF-β1 in different groups, and Western blot was used to test the expression of BRP-39 in rat lung tissue. Expression of BRP-39 increased, the fibrosis was obvious, and lung tissue collagen increased in bleomycin-induced pulmonary fibrosis in rat lung tissue. Increasing BRP-39 protein level and intratracheal bleomycin medication to establish pulmonary fibrosis model can aggravate pulmonary fibrosis. Along with the increase in BRP-39 protein level, TGF-β1 expression level also increased in lung tissue. Western blot results showed the expression of BRP-39, and TGF-β1 had the same trend in different groups. BRP-39 has effects in bleomycin-induced rat pulmonary fibrosis. Change in BRP-39 can affect the process of bleomycin-induced pulmonary fibrosis. The mechanism of BRP-3 in pulmonary fibrosis may work by regulating TGF-β1.

Keywords

Pulmonary fibrosis Bleomycin BRP-39’ TGF-β1 
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Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • Chunxian Du
    • 1
  • Yibing Yang
    • 1
  • Yuhui Lin
    • 1
  • Jiong Yang
    • 1
  1. 1.Respiratory DepartmentZhongnan Hospital of Wuhan UniversityWuhanChina

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