Affiliation:
1. Departments of Respiratory Medicine, The Third Affiliated Hospital of Soochow University
2. Departments of Intensive Care Unit, The Third Affiliated Hospital of Soochow University
Abstract
Abstract
Notoginsenoside R1 (NR1) is a main effective component of Panax notoginseng (Burk) F. H. Chen, which can inhibit lung fibroblast cell inflammatory injury. In the present study, a chronic obstructive pulmonary disease (COPD) model of BEAS-2B cells treated with cigarette smoke extract (CSE) was established in vitro to investigate the effects of NR1 on epithelial-mesenchymal transition (EMT). The results revealed that the expression levels of a-smooth muscle actin (a-SMA, a mesenchymal marker) were increased, and the levels of E-cadherin (an epithelial marker) were decreased due to exposure to CSE, which was significantly reversed by NR1. Moreover, the components of the TGF-β1/Smad pathway, including TGF-β1 and phosphorylation of Smad2 and Smad3 induced by CSE, were also downregulated through NR1. In addition, NR1 inhibited the binding activity of phosphorylated (p)-Smad2 and p-Smad3 complexes to plasminogen activator inhibitor 1. In conclusion, NR1 relieves EMT caused by CSE in BEAS-2B cells via suppressing the TGF-β1/Smad pathway.
Publisher
Research Square Platform LLC