Abstract
BackgroundThis study assessed the effects of ursolic acid (UA) on airway-vessel remodeling and muscle atrophy in cigarette smoke (CS)-induced emphysema rats and investigated potential underlying mechanisms.MethodsEmphysema was induced in a rat model with 3 months of CS exposure. Histology and immunohistochemistry (IHC) stains were used to assess airway-vessel remodeling and muscle atrophy-associated changes. Levels of cleaved-caspase3, 8-OHdG, and S100A4 were measured in airways and associated vessels to evaluate cell apoptosis, oxidant stress, epithelial-to-mesenchymal transition (EMT), and endothelial-to-mesenchymal transition (EndMT)-associated factors. Western blot and/or IHC analyses were performed to measure transforming growth factor-beta 1(TGF-β1)/Smad2.3, alpha-smooth muscle actin (α-SMA), and insulin-like growth factor 1 (IGF1) expression. We also gave cultured HBE and HUVEC cells Cigarette Smoke Extract (CSE) administration and UA intervention. Using Western blot method to measure TGF-β1/Smad2.3, α-SMA, S100A4, and IGF1 molecules expression.ResultsUA decreased oxidant stress and cell apoptosis in airway and accompanying vascular walls of cigarette smoke-induced emphysema model rats. UA alleviated EMT, EndMT, changes associated with airway-vessel remodeling and muscle atrophy. The UA effects were associated with IGF1 and TGF-β1/Smad2.3 pathways.ConclusionsUA reduced EMT, EndMT, airway-vessel remodeling, and musculi soleus atrophy in CS-induced emphysema model rats at least partly through IGF1 and TGF-β1/Smad2.3 signaling pathways.
Highlights
This study assessed the effects of ursolic acid (UA) on airway-vessel remodeling and muscle atrophy in cigarette smoke (CS)-induced emphysema rats and investigated potential underlying mechanisms
UA decreased musculi soleus atrophy in CS-induced emphysema rats We had 10 rats in each group at the beginning of the experiment, but 2 rats in the CS group died during CS exposure
In UA groups, musculi soleus atrophy related changes such as muscle cell crinkle, vacuolation, muscle fiber with Sham group, the thickness of airways and accompanying vessels were remarkably increased with CS, and UA administration alleviated these changes at all three concentrations tested (Fig. 2B)
Summary
This study assessed the effects of ursolic acid (UA) on airway-vessel remodeling and muscle atrophy in cigarette smoke (CS)-induced emphysema rats and investigated potential underlying mechanisms. Chronic obstructive pulmonary disease (COPD) is a systemic disease characterized by persistent respiratory symptoms and airway limitation. It has high prevalence and associated mortality, with a prevalence among people 40 years of age or older of 10.1% worldwide and 13.7% in China [1, 2] and was estimated to be the third leading cause of death worldwide in 2030 [3]. Muscle atrophy is an important complication of COPD [10] They are significant indicators of poor prognosis [8, 11,12,13], there are currently no effective
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