Anti-inflammatory effect of Yu-Ping-Feng-San via TGF-β1 signaling suppression in rat model of COPD

• Main Authors: Zhong-Shan Yang, Jin-Yuan Yan, Ni-Ping Han, Wei Zhou, Yu Cheng, Xiao-Mei Zhang, Ning Li, Jia-Li Yuan
• Format: Article
• Language: English
• Published: Mashhad University of Medical Sciences 2016-09-01
• Series: Iranian Journal of Basic Medical Sciences
• Subjects: COPD; Pro-inflammatory; Cytokine; TGF-β1/Smad2; YPFS
• Online Access: http://ijbms.mums.ac.ir/article_7600_7791deb9c5466e4ae548d10a9486e047.pdf
• ISSN: 2008-3866; 2008-3874

Objective(s): Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine that is widely used for treatment of the diseases in respiratory systems, including chronic obstructive pulmonary disease (COPD) recognized as chronic inflammatory disease. However, the molecular mechanism remains unclear. Here we detected the factors involved in transforming growth factor beta 1 (TGF-β1)/Smad2 signaling pathway and inflammatory cytokines, to clarify whether YPFS could attenuate inflammatory response dependent on TGF-β1/Smad2 signaling in COPD rats or cigarette smoke extract (CSE)-treated human bronchial epithelial (Beas-2B) cells.  Materials and Methods: The COPD rat model was established by exposure to cigarette smoke and intratracheal instillation of lipopolysaccharide, YPFS was administered to the animals. The efficacy of YPFS was evaluated by comparing the severity of pulmonary pathological damage, pro-inflammation cytokines, collagen related genes and the activation of TGF-β1/Smad2 signaling pathway. Furthermore, CSE-treated cells were employed to confirm whether the effect of YPFS was dependent on the TGF-β1/Smad2 signaling via knockdown Smad2 (Si-RNA), or pretreatment with the inhibitor of TGF-β1. Results: Administration of YPFS effectively alleviated injury of lung, suppressed releasing of pro-inflammatory cytokines and collagen deposition in COPD animals (P