Evidence map›Paper›PMID 19834332›Full record

ArticleJournal of cardiovascular pharmacology2010

Inhibition of soluble epoxide hydrolase by trans-4- [4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid is protective against ischemia-reperfusion injury.

Ketul R Chaudhary, Mohamed Abukhashim, Sung Hee Hwang, Bruce D Hammock, John M Seubert

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiovascular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 58 citations in OpenAlex.

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  13. EET intervention on Wnt1, NOV, and HO-1 signaling prevents obesity-induced cardiomyopathy in obese mice.American journal of physiology. Heart and circulatory physiology · 2017
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Ketul R ChaudharyFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Alberta, Canada.
Mohamed Abukhashim
Sung Hee Hwang
Bruce D Hammock
John M Seubert
University of Alberta · CAUniversity of California, Davis · US

Funding

HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR37ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1998 to 2007
$3.0M
Metabolomic study of ozone and nitronaphthalene toxicityR01ES013933 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 2005 to 2009
$1.5M
CIHR MOP79465NIEHS NIH HHS ES02710NIEHS NIH HHS R01 ES002710NIEHS NIH HHS R01 ES013933NIEHS NIH HHS R37 ES002710
6 · The paper itself

Abstract

Arachidonic acid, a polyunsaturated fatty acid, can be metabolized to cardioprotective epoxyeicosatrienoic acids (EETs) by cytochrome P450 epoxygenases, which are subsequently hydrolyzed to less bioactive dihydroxyeicosatrienoic acids by soluble epoxide hydrolase (sEH). To study the effects of pharmacological inhibitor of sEH (sEHi), C57BL6 mice hearts were perfused in Langendorff mode for 40 minutes of baseline and subjected to 30 minutes of global no-flow ischemia followed by 40 minutes of reperfusion. Hearts were perfused with the sEHi, trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB; 0.05, 0.1, 0.5, and 1 microM). To study the mechanism(s), hearts were perfused with 0.1 microM t-AUCB in the presence or absence of putative EET receptor antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (10 microM) or phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin (200 nM) or LY294002 (5 microM).Infarct size was determined at the end of 2-hour reperfusion by 2,3,5-triphenyltetrazolium chloride staining. Inhibition of sEH by t-AUCB significantly improved postischemic left ventricular developed pressure (LVDP) recovery and reduced the infarct size after ischemia and reperfusion, as compared with control hearts. Perfusion with 14,15-epoxyeicosa-5(Z)-enoic acid, wortmannin or LY294002 before ischemia abolished the cardioprotective phenotype; however, co-perfusion of both t-AUCB and 11,12-EET did not result in an additive effect on improved LVDP recovery. Together, our data suggest that pharmacological inhibition of sEH by t-AUCB is cardioprotective.

Indexed as

AnimalsArachidonic AcidBenzoatesDose-Response Relationship, DrugEicosanoidsEpoxide HydrolasesFemaleMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryReceptors, EicosanoidUrea4-(4-(3-adamantan-1-ylureido)cyclohexyloxy)benzoic acidArachidonic AcidBenzoatesEicosanoidsEpoxide HydrolasesReceptors, EicosanoidUrea

Identifiers

PMID19834332
PMCPMC2824072
OpenAlexW2163754562

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.