{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T23:58:00Z","timestamp":1784591880369,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,12,19]],"date-time":"2012-12-19T00:00:00Z","timestamp":1355875200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2013,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aim<\/jats:title><jats:p>Hepatic fibrosis is a worldwide healthy burden associated with significant morbidity and mortality. It is caused by a variety of chronic liver injuries. There is currently no effective treatment for liver fibrosis. In this report, we tested an imidazolium salt, 1,3\u2010diisopropylimidazolium tetrafluoroborate (DPIM), for its anti\u2010fibrotic properties in the thioacetamide\u2010induced mouse model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>DPIM was orally delivered to the thioacetamide\u2010treated mice via drinking water for 12 weeks at the onset of thioacetamide treatment at a concentration of 0.1% (prevention group), and for 4 weeks starting at the 8<jats:sup>th<\/jats:sup> week at a concentration of 0.1% or 0.2% (attenuation group), respectively. Messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and protein were determined by real\u2010time polymerase chain reaction and Western blotting, matrix metalloproteinase (<jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>) activities were measured by fluorogenic peptide substrate and zymography. Mitogen\u2010activated protein kinase (<jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3<jats:styled-content style=\"fixed-case\">K<\/jats:styled-content> inhibitors were applied in <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>6 cells in combination of DPIM to probe possible signal pathways underlying the compound's action.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We observed a significant reduction in collagen deposition in both prevention and attenuation groups. The \u03b1\u2010smooth muscle actin (<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>) and transforming growth factor (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>)\u2010\u03b2 gene expressions were also reduced in both groups. The reduction of collagen deposition could be in part attributed to the suppression of <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>\u20102 expression and the enhanced matrix protein remodeling by metalloproteinases, especially <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20103. <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3<jats:styled-content style=\"fixed-case\">K<\/jats:styled-content> signaling pathways may be partially participated in DPIM's molecular action.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>DPIM reduced fibrosis in the thioacetamide\u2010induced mouse liver fibrosis model, and warranted further studies for possible clinical application in the 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