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Baricitinib improves pulmonary fibrosis in mice with rheumatoid arthritis-associated interstitial lung disease by inhibiting the Jak2/Stat3 signaling pathway

Advances in rheumatology (London, England), 2023-08, Vol.63 (1), p.45-45, Article 45 [Peer Reviewed Journal]

This work is licensed under a Creative Commons Attribution 4.0 International License. ;ISSN: 2523-3106 ;EISSN: 2523-3106 ;DOI: 10.1186/s42358-023-00325-z

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  • Title:
    Baricitinib improves pulmonary fibrosis in mice with rheumatoid arthritis-associated interstitial lung disease by inhibiting the Jak2/Stat3 signaling pathway
  • Author: Liu, Hongli ; Yang, Yan ; Zhang, Jie ; Li, Xuelin
  • Subjects: Baricitinib ; Interstitial lung disease ; Jak2/Stat3 ; Rheumatoid arthritis ; RHEUMATOLOGY
  • Is Part Of: Advances in rheumatology (London, England), 2023-08, Vol.63 (1), p.45-45, Article 45
  • Description: Abstract Objective The study explored improvements in pulmonary inflammation and fibrosis in a bovine type II collagen-induced rheumatoid arthritis-associated interstitial lung disease mouse model after treatment with baricitinib and the possible mechanism of action. Methods A rheumatoid arthritis-associated interstitial lung disease mouse model was established, siRNA Jak2 and lentiviral vectors were transfected with human embryonic lung fibroblast cells. And the levels of relevant proteins in mouse lung tissue and human embryonic lung fibroblasts were detected by Western blotting. Results The levels of JAK2, p-JAK2, p-STAT3, p-SMAD3, SMA, TGFβR2, FN and COL4 were increased in the lung tissues of model mice ( P < 0.5) and decreased after baricitinib intervention ( P < 0.05). The expression levels of p-STAT3, p-SMAD3, SMA, TGFβR2, FN and COL4 were reduced after siRNA downregulation of the JAK2 gene ( P < 0.01) and increased after lentiviral overexpression of the JAK2 gene ( P < 0.01). Conclusion Baricitinib alleviated fibrosis in the lung tissue of rheumatoid arthritis-associated interstitial lung disease mice, and the mechanism of action may involve the downregulation of Smad3 expression via inhibition of the Jak2/Stat3 signaling pathway, with consequent inhibition of the profibrotic effect of transforming growth factor-β1.
  • Publisher: Sociedade Brasileira de Reumatologia
  • Language: English;Portuguese
  • Identifier: ISSN: 2523-3106
    EISSN: 2523-3106
    DOI: 10.1186/s42358-023-00325-z
  • Source: SciELO
    ProQuest Central
    DOAJ Directory of Open Access Journals
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