ArticleImmunity, inflammation and disease2024
Forsythiaside A ameliorates bleomycin-induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Forsythiaside A inhibits the progression of intrahepatic cholangiocarcinoma partially via suppressing oxidative stress-induced hepatic stellate cell activation and macrophage polarization.BMC biotechnology · 2026Article
- The Mechanism of Oxidative Stress in Pulmonary Fibrosis and Research Progress.Antioxidants (Basel, Switzerland) · 2026Review
- Anti-ovarian cancer effects of forsythiaside A: insights fromTranslational cancer research · 2025Article
- Forsythiaside A ameliorates bleomycin-induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis.Immunity, inflammation and disease · 2024Article
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5 authors.
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Abstract
backgroundPulmonary fibrosis (PF) is a common clinically critical disease characterized by high morbidity and high mortality. Forsythiaside A (FA) is a phenylethanol glycoside component in Forsythia suspensa, which has anti-inflammatory, antioxidant, and antiviral activities. However, the effects of FA on bleomycin (BLM)-induced PF are unclear. PURPOSE: The present study explored the role of FA in the amelioration of oxidative stress and apoptosis in BLM-induced PF as well as the possible underlying mechanisms, in vivo and in vitro.
methodsNetwork pharmacology was used to collect the effects of FA on BLM-induced PF. Subsequently, further observation of the effects of FA on mice with PF by pulmonary pathological changes, transmission electron microscopy, real-time polymerase chain reaction, Western blot analysis, immunofluorescence, and immunohistochemistry. An in vitro model was constructed by inducing A549 with transforming growth factor beta-1 (TGF-β1) to observe the effect of FA on epithelial cell apoptosis.
resultsNetwork pharmacology predicted signaling pathways such as IL-17 signaling pathway and Relaxin signaling pathway. The results of in vivo studies showed that FA ameliorated BLM-induced PF through inhibition of fibrosis, modulation of apoptosis, and oxidative stress. In addition, FA promoted TGF-β1-induced apoptosis in A549 cells.
conclusionsThe results of our study suggested that FA could protect mice against BLM-induced PF by regulating oxidative stress and apoptosis as well as the Epithelial mesenchymal transition pathway.
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