Anti-fibrotic effect of thalidomide through inhibiting TGF-beta-induced ERK1/2 pathways in bleomycin-induced lung fibrosis in mice
- Authors
- Choe, Jung-Yoon; Jung, Hyun-Joo; Park, Ki-Yeun; Kum, Yoon-Seup; Song, Gwan Gyu; Hyun, Dae-Sung; Park, Sung-Hoon; Kim, Seong-Kyu
- Issue Date
- 3월-2010
- Publisher
- SPRINGER BASEL AG
- Keywords
- Thalidomide; Bleomycin; Lung; Fibrosis; TGF-beta; ERK1/2
- Citation
- INFLAMMATION RESEARCH, v.59, no.3, pp.177 - 188
- Indexed
- SCIE
SCOPUS
- Journal Title
- INFLAMMATION RESEARCH
- Volume
- 59
- Number
- 3
- Start Page
- 177
- End Page
- 188
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/116839
- DOI
- 10.1007/s00011-009-0084-9
- ISSN
- 1023-3830
- Abstract
- This study is designed to confirm the anti-fibrotic effect of thalidomide on bleomycin-induced lung fibrosis in a mouse model and to identify whether this anti-fibrotic effect is associated with inhibition of the transforming growth factor-beta (TGF-beta)-induced extracellular signal-regulated kinase1/2 (ERK1/2). C57BL/6 female mice were administered blomycin sulfate. In cultured human lung fibroblasts, expressions of type I collagen, fibronectin, and either TGF-beta or IL-6 were measured after thalidomide treatment by reverse transcription-polymerase chain reaction (RT-PCR). Expressions of ERK1/2, type I collagen, fibronectin, and TGF-beta 1 from lung tissues of blomycin-induced mice and from mouse lung fibroblasts were evaluated using RT-PCR and western blotting. Thalidomide administration significantly inhibits TGF-beta 1 mRNA expression in a dose-dependant manner following administration of IL-6 and IL-6R. In the analysis of BAL fluids, total BAL inflammatory cell counts, TGF-beta 1, and IL-6 levels in thalidomide-treated mice were significantly reduced when compared with bleomycin-treated mice (p < 0.01, p < 0.01, and p < 0.001, respectively). Thalidomide inhibited total ERK1/2 and phospho-ERK1/2 expression after TGF-beta 1 stimulation in the RT-PCR and western blotting. The results of our study suggest that the anti-fibrotic effect of thalidomide on lung fibrosis may be related to suppression of the TGF-beta 1-induced ERK1/2 signaling pathway.
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