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10.1155/2017/7171404 http://scihub22266oqcxt.onion/10.1155/2017/7171404 C5572594!5572594 !29104873     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29104873 &cmd=llinks): Failed to open stream: HTTP request failed! 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Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-?1/Smad Pathway |pdf=|usr=}}{{29104873 }} gab.com Text Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF- 1/Smad Pathway JO: Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=29104873 #FOAvip Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. 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 ?-smooth muscle actin (?-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-?1/Smad pathway components, including TGF-?1, TGF-?R1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-?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-?1/Smad pathway. Twit Text FOAVip Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF- 1/Smad Pathway ????Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=29104873 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29104873 #FOAvip English Wikipedia <ref>{{Cite pmid|29104873 }}</ref> Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-?1/Smad Pathway #MMPMID29104873 Guan S ; Xu W ; Han F ; Gu W ; Song L ; Ye W ; Liu Q ; Guo X Biomed Res Int 2017[]; 2017 (ä): 7171404 PMID29104873 show ga Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. 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 ?-smooth muscle actin (?-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-?1/Smad pathway components, including TGF-?1, TGF-?R1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-?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-?1/Smad pathway. |Actins/genetics [MESH] |Animals [MESH] |Bronchi/drug effects/pathology [MESH] |Cadherins/genetics [MESH] |Cigarette Smoking/adverse effects [MESH] |Epithelial-Mesenchymal Transition/drug effects/genetics [MESH] |Ginsenosides/*administration & dosage [MESH] |Humans [MESH] |Imidazoles/administration & dosage [MESH] |Lung/metabolism/pathology [MESH] |Pulmonary Disease, Chronic Obstructive/chemically induced/*drug therapy/genetics/pathology [MESH] |Quinoxalines/administration & dosage [MESH] |Rats [MESH] |Signal Transduction/drug effects [MESH] |Smad2 Protein/*genetics [MESH] |Smad3 Protein/*genetics [MESH]Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithel(epmc).pdf DeepDyve Pubget Overpricing