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Long\u2010term administration of celecoxib, a selective cyclooxygenase\u20102 (<jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102) inhibitor, can ameliorate hepatic fibrosis. This research aimed to examine the effect of celecoxib on the <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> of hepatocytes during the development of liver cirrhosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Cirrhotic liver model of rat was established by peritoneal injection of thiacetamide (<jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content>). Thirty\u2010six rats were randomly assigned to control, <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content>\u2009+\u2009celecoxib groups. Hepatic expressions of tumor necrosis factor\u2010\u03b1 (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1), interleukin 6 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106), <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102, prostaglandin <jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><jats:sub>2<\/jats:sub> (<jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub>), matrix metalloproteinase (MMP)\u20102 and \u20109, transforming growth factor\u2010\u03b21 (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21), <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>hospho\u2010<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>mad2\/3, <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>nail1, \u03b1\u2010smooth muscle actin (\u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>), vimentin, collagen <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>, fibroblast\u2010specific protein (<jats:styled-content style=\"fixed-case\">FSP<\/jats:styled-content>\u20101), <jats:italic><jats:styled-content style=\"fixed-case\">E<\/jats:styled-content><\/jats:italic>\u2010cadherin and <jats:italic><jats:styled-content style=\"fixed-case\">N<\/jats:styled-content><\/jats:italic>\u2010cadherin were quantitated. Hepatic fibrosis was assessed by the visible hepatic fibrotic areas and <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>shak's scoring system.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Exposed to <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content> treatment, hepatocytes underwent the process of <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> during hepatic fibrosis. Compared with those in <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content> group, celecoxib significantly downregulated the hepatic expressions of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102, <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content><jats:sub>2<\/jats:sub>, <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20102, <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20109, <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21, <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>hospho\u2010<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>mad2\/3, <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>nail1, \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">FSP<\/jats:styled-content>\u20101, and vimentin while greatly restoring the levels of <jats:italic><jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>\u2010<\/jats:italic>cadherin. The fibrotic areas and collagen <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content> levels of <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content>\u2009+\u2009celecoxib group were much lower than those in <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content> group.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Celecoxib could ameliorate hepatic fibrosis and cirrhosis in <jats:styled-content style=\"fixed-case\">TAA<\/jats:styled-content>\u2010rat model through suppression of the mesenchymal biomarkers in the hepatocytes while restoring the levels of their epithelial biomarkers. The inhibitory effect of celecoxib on the <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> of hepatocytes is associated with reduction of intrahepatic inflammation, preservation of normal basement matrix, and inhibition of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u2010\u03b21\/<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>mad pathway.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.12641","type":"journal-article","created":{"date-parts":[[2014,6,9]],"date-time":"2014-06-09T10:55:27Z","timestamp":1402311327000},"page":"1932-1942","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Celecoxib attenuates hepatic cirrhosis through inhibition of epithelial\u2010to\u2010mesenchymal transition of hepatocytes"],"prefix":"10.1111","volume":"29","author":[{"given":"Shi\u2010Lei","family":"Wen","sequence":"first","affiliation":[{"name":"Regenerative Medicine Research Center West China Hospital  Chengdu China"},{"name":"Division of Peptides Related with Human Diseases State Key Laboratory of Biotherapy Sichuan University  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin\u2010Hang","family":"Gao","sequence":"additional","affiliation":[{"name":"Division of Peptides Related with Human Diseases State Key Laboratory of Biotherapy Sichuan University  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen\u2010Juan","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology West China Hospital  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao\u2010Yao","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology West China Hospital  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huan","family":"Tong","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology West China Hospital  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi\u2010Yin","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology West China Hospital  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhang\u2010Xu","family":"Liu","sequence":"additional","affiliation":[{"name":"Research Center for Liver Diseases Keck School of Medicine University of Southern California  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheng\u2010Wei","family":"Tang","sequence":"additional","affiliation":[{"name":"Division of Peptides Related with Human Diseases State Key Laboratory of Biotherapy Sichuan University  Chengdu China"},{"name":"Department of Gastroenterology West China Hospital  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,11,13]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-pathol-011110-130246"},{"issue":"1","key":"e_1_2_6_3_1","doi-asserted-by":"crossref","first-page":"S26","DOI":"10.1186\/1755-1536-5-S1-S26","article-title":"Reversibility of liver fibrosis","volume":"5","author":"Pellicoro A","year":"2012","journal-title":"Fibrogenesis. 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