BMC pulmonary medicine, 2024-05, Vol.24 (1), p.229-229
2024
Details
- Autor(en) / Beteiligte
- Titel
- Sinomenine attenuates pulmonary fibrosis by downregulating TGF-β1/Smad3, PI3K/Akt and NF-κB signaling pathways
- Ist Teil von
- BMC pulmonary medicine, 2024-05, Vol.24 (1), p.229-229
- Ort / Verlag
- England: BioMed Central
- Erscheinungsjahr
- 2024
- Link zum Volltext
- Quelle
- SpringerLink (Online service)
- Beschreibungen/Notizen
- Since COVID-19 became a global epidemic disease in 2019, pulmonary fibrosis (PF) has become more prevalent among persons with severe infections, with IPF being the most prevalent form. In traditional Chinese medicine, various disorders are treated using Sinomenine (SIN). The SIN's strategy for PF defense is unclear. Bleomycin (BLM) was used to induce PF, after which inflammatory factors, lung histological alterations, and the TGF-/Smad signaling pathway were assessed. By administering various dosages of SIN and the TGF- receptor inhibitor SB-431,542 to human embryonic lung fibroblasts (HFL-1) and A549 cells, we were able to examine proliferation and migration as well as the signaling molecules implicated in Epithelial-Mesenchymal Transition (EMT) and Extra-Cellular Matrix (ECM). In vivo, SIN reduced the pathological changes in the lung tissue induced by BLM, reduced the abnormal expression of inflammatory cytokines, and improved the weight and survival rate of mice. In vitro, SIN inhibited the migration and proliferation by inhibiting TGF-β1/Smad3, PI3K/Akt, and NF-κB pathways, prevented the myofibroblasts (FMT) of HFL-1, reversed the EMT of A549 cells, restored the balance of matrix metalloenzymes, and reduced the expression of ECM proteins. SIN attenuated PF by down-regulating TGF-β/Smad3, PI3K/Akt, and NF-κB signaling pathways, being a potential effective drug in the treatment of PF.
- Sprache
- Englisch
- Identifikatoren
- eISSN: 1471-2466DOI: 10.1186/s12890-024-03050-5Titel-ID: cdi_doaj_primary_oai_doaj_org_article_6d6f1f0436c84e42a7c4409d1f5112a8
- Format
- –
- Schlagworte
- 1-Phosphatidylinositol 3-kinase, A549 Cells, AKT protein, Animals, Bleomycin, Cell Movement - drug effects, Cell proliferation, Cell Proliferation - drug effects, Cells, Coronaviruses, COVID-19, Cytokines, Disease Models, Animal, Down-Regulation, Drugs, Embryo fibroblasts, Epithelial-Mesenchymal Transition - drug effects, Extracellular matrix, Fibrosis, Humans, Inflammation, Laboratory animals, Liver, Lung - drug effects, Lung - pathology, Lung diseases, Lungs, Male, Medical research, Mice, Mice, Inbred C57BL, Morphinans - pharmacology, Morphinans - therapeutic use, NF-kappa B - metabolism, NF-κB, NF-κB protein, Phosphatidylinositol 3-Kinases - metabolism, PI3K/Akt, Pneumonia, Proto-Oncogene Proteins c-akt - metabolism, Pulmonary fibrosis, Pulmonary Fibrosis - drug therapy, Pulmonary Fibrosis - metabolism, Signal transduction, Signal Transduction - drug effects, Sinomenine, Smad protein, Smad3 protein, Smad3 Protein - metabolism, TGF-β1/Smad3, Traditional Chinese medicine, Transforming Growth Factor beta1 - metabolism, Transforming growth factor-b, Transforming growth factor-b1, Tumor necrosis factor-TNF, Wound healing