ArticleSarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG2024
Schisandrin B attenuates bleomycin-induced pulmonary fibrosis in mice through AKT-mTOR pathway.
Article in Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Schisandrin B confers multi-organ protection via regulation of mitochondrial homeostasis: mechanistic integration, organ-specific differences, and translational challenges-a review.Frontiers in pharmacology · 2026Review
- 3,5,6,7,8,3',4'- Heptamethoxyflavonoid inhibits TGF-β1-induced epithelial-mesenchymal transition by regulating oxidative stress and autophagy through MEK/ERK/PI3K/AKT/mTOR signaling pathway.Scientific reports · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSchisandrin B (Sch B) is an active monomer of Schisandrin with anti-fibrosis pharmacological action. The study investigated whether Sch B alleviate bleomycin-induced (BLM-Induced) pulmonary fibrosis in mice and attempted to clarify its anti-fibrosis mechanism.
methodsHistopathological examination was performed by H&E staining and immunohistochemistry. The inflammatory cytokines and oxidative stress were determined by ELISA. Western blotting and immunofluorescence were used to investigate the possible molecular mechanism to attenuate pulmonary fibrosis by Sch B.
resultsThe results indicated that Sch B can significantly attenuate BLM-Induced pulmonary fibrosis, myofibroblast activation, and collagen fibers deposition in mice. In addition, Sch B can inhibit inflammatory response and oxidative stress in early stage. Furthermore, Sch B can inhibit pulmonary fibrosis by promoting autophagy via promoting the dephosphorylation of AKT-mTOR pathway.
conclusionsThe results suggest that the anti-fibrotic effect of Sch B is potentially related to the activation of autophagy through AKT-mTOR pathway, and Sch B is a potential agent for the treatment of idiopathic pulmonary fibrosis.
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Registered trials
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