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Forsythiaside A Ameliorates Bleomycin-induced Pulmonary Fibrosis by Inhibiting Oxidative Stress and Apoptosis

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Abstract

Background: Pulmonary 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.

Methods: Network 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.

Results: Network 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.

Conclusions: The 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.

Citing Articles

Forsythiaside A ameliorates bleomycin-induced pulmonary fibrosis by inhibiting oxidative stress and apoptosis.

Yang F, Zhang Q, Wang X, Hu Y, Chen S Immun Inflamm Dis. 2024; 12(8):e70006.

PMID: 39172055 PMC: 11340632. DOI: 10.1002/iid3.70006.

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