{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,17]],"date-time":"2025-12-17T06:42:20Z","timestamp":1765953740780,"version":"3.48.0"},"reference-count":35,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,12,17]],"date-time":"2025-12-17T00:00:00Z","timestamp":1765929600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>To investigate the effect of urotensin II(UII)\/UII receptor(UT) on hepatic carboxylesterase1f(Ces1f) expression in acute liver failure(ALF) mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      ALF was induced in male Balb\/c mice using lipopolysaccharide (LPS)\/D-galactosamine (D-GalN) i.p. after a tail vein injection of Urantide, a specific antagonist of UT receptor. Liver tissues were collected at 0-12h to detect\n                      <jats:italic>UII<\/jats:italic>\n                      and\n                      <jats:italic>Ces1f<\/jats:italic>\n                      mRNA levels in ALF mice. Mice were divided into four groups (n=6 each group): (A) Urantide(-), LPS\/D-GalN(-), (B) Urantide(+), LPS\/D-GalN(-), (C) Urantide(-), LPS\/D-GalN(+), and (D) Urantide(+), LPS\/D-GalN(+). Liver tissues were collected at 6 h after a challenge of LPS\/D-GalN. Time-depended levels were observed of hepatic\n                      <jats:italic>UII<\/jats:italic>\n                      and\n                      <jats:italic>Ces1f<\/jats:italic>\n                      mRNA over a period of 12 hours after LPS\/D-GalN challenge. Liver injury was evaluated via hematoxylin-eosin (HE) staining, serum alanine aminotransferase(ALT)\/aspartate aminotransferase(AST), and the mRNA and protein expression levels of Ces1f and UII expression were determined by fluorescence\n                      <jats:italic>in situ<\/jats:italic>\n                      hybridization(FISH), quantitative real-time PCR (qPCR) and Western blotting (WB), respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      After LPS\/D-GalN injection, hepatic\n                      <jats:italic>UII<\/jats:italic>\n                      mRNA rose at 2 h (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt; 0.05\n                      <jats:italic>vs<\/jats:italic>\n                      0 h), reached the peaked level at 6 h, and the level began to degrade at 8 h, but remained higher than at 0 h (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt; 0.05, 10 h\n                      <jats:italic>vs<\/jats:italic>\n                      0 h) till 12 h (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;gt;0.05, 12 h\n                      <jats:italic>vs<\/jats:italic>\n                      0 h); while hepatic\n                      <jats:italic>Ces1f<\/jats:italic>\n                      mRNA decreased at 6 h (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt; 0.05\n                      <jats:italic>vs<\/jats:italic>\n                      0 h), reached the lowest level at 10 h, but began to rise at 12 h (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;gt;0.05, 12 h\n                      <jats:italic>vs<\/jats:italic>\n                      10 h). In addition, urantide pretreatment inhibited the up-regulated expressions of hepatic\n                      <jats:italic>UII<\/jats:italic>\n                      mRNA and protein, whereas increases the down-regulated expressions of hepatic\n                      <jats:italic>Ces1f<\/jats:italic>\n                      mRNA and protein induced by LPS\/D-GalN attack at 6 h.And serum ALT and AST levels were significantly decreased, whereas hepatic inflammatory injury improved via urantide injection in LPS\/D-GalN-induced ALF mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Ces1f maybe negatively regulated by UII\/UT signal in LPS\/D-GalN-induced ALF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcimb.2025.1653725","type":"journal-article","created":{"date-parts":[[2025,12,17]],"date-time":"2025-12-17T06:37:43Z","timestamp":1765953463000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Urantide alleviates lipopolysaccharide\/D-galactosamine-induced acute liver failure through upregulating carboxylesterase1f in mice"],"prefix":"10.3389","volume":"15","author":[{"given":"Wanhua","family":"Yang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shu","family":"Bian","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Liangming","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2025,12,17]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"1564","DOI":"10.1002\/hep.26933","article-title":"Secretory leukocyte protease inhibitor: a pivotal mediator of anti-inflammatory responses in acetaminophen-induced acute liver failure","volume":"59","author":"Antoniades","year":"2014","journal-title":"Hepatology."},{"key":"B2","doi-asserted-by":"publisher","first-page":"984","DOI":"10.1016\/j.celrep.2018.12.094","article-title":"Impaired LXR\u03b1 Phosphorylation attenuates progression of fatty liver disease","volume":"26","author":"Becares","year":"2019","journal-title":"Cell Rep."},{"key":"B3","doi-asserted-by":"publisher","first-page":"43","DOI":"10.1124\/dmd.121.000649","article-title":"Transcriptional regulation of carboxylesterase 1 in human liver: role of the nuclear receptor subfamily 1 group H member 3 and its splice isoforms","volume":"50","author":"Collins","year":"2022","journal-title":"Drug Metab. 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