{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:32:49Z","timestamp":1791300769433,"version":"4.1.0"},"reference-count":62,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,3,25]],"date-time":"2013-03-25T00:00:00Z","timestamp":1364169600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,4]]},"abstract":"Background and Purpose<\/jats:title>We have previously shown that isoprenaline\u2010induced cardiac hypertrophy causes significant changes in the expression of cytochromes P450<\/jats:styled-content> (CYP<\/jats:styled-content>) and soluble epoxide hydrolase (sEH<\/jats:styled-content>) genes. Therefore, it is important to examine whether the inhibition of sEH<\/jats:styled-content> by 1\u2010(1\u2010methanesulfonyl\u2010piperidin\u20104\u2010yl)\u20103\u2010(4\u2010trifluoromethoxy\u2010phenyl)\u2010urea (TUPS<\/jats:styled-content>) will protect against isoprenaline\u2010induced cardiac hypertrophy.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>Male S<\/jats:styled-content>prague\u2013D<\/jats:styled-content>awley rats were treated with TUPS<\/jats:styled-content> (0.65\u2009mg\u2009kg\u22121<\/jats:sup>\u2009day\u22121<\/jats:sup>, p.o.), isoprenaline (5\u2009mg\u2009kg\u22121<\/jats:sup>\u2009day\u22121<\/jats:sup>, i.p.) or the combination of both. In vitro<\/jats:italic>\u2005H9c2<\/jats:styled-content> cells were treated with isoprenaline (100 \u03bcM<\/jats:styled-content>) in the presence and absence of either TUPS<\/jats:styled-content> (1 \u03bcM<\/jats:styled-content>) or 11,12 EET<\/jats:styled-content> (1 \u03bcM<\/jats:styled-content>). The expression of hypertrophic, fibrotic markers and different CYP<\/jats:styled-content><\/jats:italic> genes were determined by real\u2010time PCR.<\/jats:p><\/jats:sec>Key Results<\/jats:title>Isoprenaline significantly induced the hypertrophic, fibrotic markers as well as the heart to body weight ratio, which was significantly reversed by TUPS<\/jats:styled-content>. Isoprenaline also caused an induction of CYP1A1<\/jats:styled-content><\/jats:italic>, CYP1B1<\/jats:styled-content><\/jats:italic>, CYP2B1<\/jats:styled-content><\/jats:italic>, CYP2B2<\/jats:styled-content><\/jats:italic>, CYP4A3<\/jats:styled-content><\/jats:italic> and CYP4F4<\/jats:styled-content><\/jats:italic> gene expression and TUPS<\/jats:styled-content> significantly inhibited this isoprenaline\u2010mediated effect. Moreover, isoprenaline significantly reduced 5,6\u2010, 8,9\u2010, 11,12\u2010 and 14,15\u2010EET<\/jats:styled-content> and increased their corresponding 8,9\u2010, 11,12\u2010 and 14,15\u2010dihydroxyeicosatrienoic acid (DHET<\/jats:styled-content>) and the 20\u2010HETE<\/jats:styled-content> metabolites. TUPS<\/jats:styled-content> abolished these isoprenaline\u2010mediated changes in arachidonic acid (AA<\/jats:styled-content>) metabolites. In H9c2<\/jats:styled-content> cells, isoprenaline caused a significant induction of ANP<\/jats:styled-content>, BNP<\/jats:styled-content> and EPHX2 mRNA<\/jats:styled-content> levels. Both TUPS<\/jats:styled-content> and 11,12\u2010EET<\/jats:styled-content> significantly decreased this isoprenaline\u2010mediated induction of ANP<\/jats:styled-content>, BNP<\/jats:styled-content> and EPHX2<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>TUPS<\/jats:styled-content> partially protects against isoprenaline\u2010induced cardiac hypertrophy, which confirms the role of sEH and CYP<\/jats:styled-content> enzymes in the development of cardiac hypertrophy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.12066","type":"journal-article","created":{"date-parts":[[2012,11,26]],"date-time":"2012-11-26T09:51:39Z","timestamp":1353923499000},"page":"1794-1807","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["Soluble epoxide hydrolase inhibitor, TUPS<\/scp>, protects against isoprenaline\u2010induced cardiac hypertrophy"],"prefix":"10.1111","volume":"168","author":[{"given":"Hassan N","family":"Althurwi","sequence":"first","affiliation":[{"name":"Faculty of Pharmacy and Pharmaceutical Sciences University of Alberta Edmonton AB Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mandy MY","family":"Tse","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy and Pharmaceutical Sciences University of Alberta Edmonton AB Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ghada","family":"Abdelhamid","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy and Pharmaceutical Sciences University of Alberta Edmonton AB Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beshay NM","family":"Zordoky","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy and Pharmaceutical Sciences University of Alberta Edmonton AB Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce D","family":"Hammock","sequence":"additional","affiliation":[{"name":"Department of Entomology Cancer Research Center University of California Davis CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayman OS","family":"El\u2010Kadi","sequence":"additional","affiliation":[{"name":"Faculty of Pharmacy and Pharmaceutical Sciences University of Alberta Edmonton AB 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