Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease. There are no effective drug therapies for IPF. Hyperoside, a flavonoid glycoside, has been proven to have anti-inflammatory, anti-fibrosis, antioxidant, and anti-cancer effects. The aim of this study was to explore the role of hyperoside in bleomycin-induced pulmonary fibrosis development in mice. We established the pulmonary fibrosis model by a single intratracheal aerosol injection of bleomycin. Seven days after the bleomycin treatment, the mice were intraperitoneally administered with hyperoside for 14 days. We found that hyperoside treatment ameliorated fibrotic pathological changes and collagen deposition in the lungs of mice with bleomycin-induced pulmonary fibrosis. Hyperoside treatment also reduced the levels of MDA, TNF-α, and IL-6 and increased the activity of SOD. In addition, hyperoside might inhibit the epithelial-mesenchymal transition (EMT) via the AKT/GSK3β pathway. Based on these findings, hyperoside attenuated pulmonary fibrosis development by inhibiting oxidative stress, inflammation, and EMT in the lung tissues of mice with pulmonary fibrosis. Therefore, hyperoside might be a promising candidate drug for the treatment of pulmonary fibrosis.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease (Kim et al, 2015)
IPF is characterized by aberrant alveolar epithelial cells, uncontrolled myofibroblast proliferation, and abnormal extracellular matrix (ECM) deposition (Richeldi et al, 2017)
We explored the protective effects of Hyp on Blm-induced pulmonary fibrosis in a C57BL/6 mice model
Summary
Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease (Kim et al, 2015). IPF patients have poor long-term survival (Scotton and Chambers, 2007). EMT plays an important role in many respiratory diseases, including pulmonary fibrosis (Marmai et al, 2011), chronic obstructive pulmonary disease (Xu et al, 2017), and lung cancer (Yin et al, 2020). This transition includes the loss of epithelial markers and the acquisition of mesenchymal markers, which leads to functional changes, including cell migration, invasion, and cell cycle arrest (Willis and Borok, 2007; Lovisa et al, 2015; Yang et al, 2020). Pirfenidone and nintedanib, which have been approved by the FDA for treating IPF patients, may be able to alleviate the development of IPF, they provide only
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