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Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS) and human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE). Our data showed that CS or CSE exposure increased expression of the mesenchymal marker<jats:italic>\u03b1<\/jats:italic>-smooth muscle actin (<jats:italic>\u03b1<\/jats:italic>-SMA) and decreased expression of the epithelial marker epithelial cadherin (E-cad) in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-<jats:italic>\u03b2<\/jats:italic>1\/Smad pathway components, including TGF-<jats:italic>\u03b2<\/jats:italic>1, TGF-<jats:italic>\u03b2<\/jats:italic>R1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-<jats:italic>\u03b2<\/jats:italic>R1-Smad2\/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-<jats:italic>\u03b2<\/jats:italic>1\/Smad pathway.<\/jats:p>","DOI":"10.1155\/2017\/7171404","type":"journal-article","created":{"date-parts":[[2017,8,13]],"date-time":"2017-08-13T17:03:21Z","timestamp":1502643801000},"page":"1-12","source":"Crossref","is-referenced-by-count":34,"title":["Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-<i>\u03b2<\/i>1\/Smad Pathway"],"prefix":"10.1155","volume":"2017","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7728-1128","authenticated-orcid":true,"given":"Sibin","family":"Guan","sequence":"first","affiliation":[{"name":"Department of Respiratory Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, 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