Bibliographic Details
| Title: |
Tauroursodeoxycholic acid alleviates pulmonary endoplasmic reticulum stress and epithelial-mesenchymal transition in bleomycin-induced lung fibrosis |
| Authors: |
Bin Tong, Lin Fu, Biao Hu, Zhi-Cheng Zhang, Zhu-Xia Tan, Se-Ruo Li, Yuan-Hua Chen, Cheng Zhang, Hua Wang, De-Xiang Xu, Hui Zhao |
| Source: |
BMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-11 (2021) |
| Publisher Information: |
BMC, 2021. |
| Publication Year: |
2021 |
| Collection: |
LCC:Diseases of the respiratory system |
| Subject Terms: |
Idiopathic pulmonary fibrosis, Tauroursodeoxycholic acid, Epithelial-mesenchymal transition, Endoplasmic reticulum stress, Oxidative stress, Diseases of the respiratory system, RC705-779 |
| More Details: |
Abstract Background Several studies demonstrate that endoplasmic reticulum (ER) stress-mediated epithelial-mesenchymal transition (EMT) is involved in the process of bleomycin (BLM)-induced pulmonary fibrosis. Tauroursodeoxycholic acid (TUDCA), a bile acid with chaperone properties, is an inhibitor of ER stress. This study aimed to investigate the preventive effects of TUDCA on BLM-induced EMT and lung fibrosis. Methods The model of lung fibrosis was established by intratracheal injection with a single dose of BLM (3.0 mg/kg). In TUDCA + BLM group, mice were intraperitoneally injected with TUDCA (250 mg/kg) daily. Results BLM-induced alveolar septal destruction and inflammatory cell infiltration were alleviated by TUDCA. BLM-induced interstitial collagen deposition, as determined by Sirius Red staining, was attenuated by TUDCA. BLM-induced elevation of pulmonary α-smooth muscle actin (α-SMA) and reduction of pulmonary E-cadherin were attenuated by TUDCA. BLM-induced pulmonary Smad2/3 phosphorylation was suppressed by TUDCA. BLM-induced elevation of Ki67 and PCNA was inhibited by TUDCA in mice lungs. In addition, BLM-induced elevation of HO-1 (heme oxygenase-1) and 3-NT (3-nitrotyrosine) was alleviated by TUDCA. Finally, BLM-induced upregulation of pulmonary GRP78 and CHOP was attenuated by TUDCA. Conclusions These results provide evidence that TUDCA pretreatment inhibits Smad2/3-medited EMT and subsequent lung fibrosis partially through suppressing BLM-induced ER stress and oxidative stress. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
1471-2466 |
| Relation: |
https://doaj.org/toc/1471-2466 |
| DOI: |
10.1186/s12890-021-01514-6 |
| Access URL: |
https://doaj.org/article/837e52fd33934390ad7c815fb33886c3 |
| Accession Number: |
edsdoj.837e52fd33934390ad7c815fb33886c3 |
| Database: |
Directory of Open Access Journals |
