Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Epoxyeicosatrienoic acid analog EET-B attenuates post-myocardial infarction remodeling in spontaneously hypertensive rats

J. Neckář, MA. Hye Khan, GJ. Gross, M. Cyprová, J. Hrdlička, A. Kvasilová, JR. Falck, WB. Campbell, L. Sedláková, Š. Škutová, V. Olejníčková, M. Gregorovičová, D. Sedmera, F. Kolář, JD. Imig,

. 2019 ; 133 (8) : 939-951. [pub] 20190429

Language English Country Great Britain

Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

Grant support
R01 DK103616 NIDDK NIH HHS - United States
R01 HL111392 NHLBI NIH HHS - United States
R01 HL132908 NHLBI NIH HHS - United States
NV15-27735A MZ0 CEP Register

Epoxyeicosatrienoic acids (EETs) and their synthetic analogs have cardiovascular protective effects. Here, we investigated the action of a novel EET analog EET-B on the progression of post-myocardial infarction (MI) heart failure in spontaneously hypertensive rats (SHR). Adult male SHR were divided into vehicle- and EET-B (10 mg/kg/day; p.o., 9 weeks)-treated groups. After 2 weeks of treatment, rats were subjected to 30-min left coronary artery occlusion or sham operation. Systolic blood pressure (SBP) and echocardiography (ECHO) measurements were performed at the beginning of study, 4 days before, and 7 weeks after MI. At the end of the study, tissue samples were collected for histological and biochemical analyses. We demonstrated that EET-B treatment did not affect blood pressure and cardiac parameters in SHR prior to MI. Fractional shortening (FS) was decreased to 18.4 ± 1.0% in vehicle-treated MI rats compared with corresponding sham (30.6 ± 1.0%) 7 weeks following MI induction. In infarcted SHR hearts, EET-B treatment improved FS (23.7 ± 0.7%), markedly increased heme oxygenase-1 (HO-1) immunopositivity in cardiomyocytes and reduced cardiac inflammation and fibrosis (by 13 and 19%, respectively). In conclusion, these findings suggest that EET analog EET-B has beneficial therapeutic actions to reduce cardiac remodeling in SHR subjected to MI.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc20006463
003      
CZ-PrNML
005      
20220530145437.0
007      
ta
008      
200511s2019 xxk f 000 0|eng||
009      
AR
024    7_
$a 10.1042/CS20180728 $2 doi
035    __
$a (PubMed)30979784
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxk
100    1_
$a Neckář, Jan $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, U.S.A. jan.neckar@fgu.cas.cz. Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
245    10
$a Epoxyeicosatrienoic acid analog EET-B attenuates post-myocardial infarction remodeling in spontaneously hypertensive rats / $c J. Neckář, MA. Hye Khan, GJ. Gross, M. Cyprová, J. Hrdlička, A. Kvasilová, JR. Falck, WB. Campbell, L. Sedláková, Š. Škutová, V. Olejníčková, M. Gregorovičová, D. Sedmera, F. Kolář, JD. Imig,
520    9_
$a Epoxyeicosatrienoic acids (EETs) and their synthetic analogs have cardiovascular protective effects. Here, we investigated the action of a novel EET analog EET-B on the progression of post-myocardial infarction (MI) heart failure in spontaneously hypertensive rats (SHR). Adult male SHR were divided into vehicle- and EET-B (10 mg/kg/day; p.o., 9 weeks)-treated groups. After 2 weeks of treatment, rats were subjected to 30-min left coronary artery occlusion or sham operation. Systolic blood pressure (SBP) and echocardiography (ECHO) measurements were performed at the beginning of study, 4 days before, and 7 weeks after MI. At the end of the study, tissue samples were collected for histological and biochemical analyses. We demonstrated that EET-B treatment did not affect blood pressure and cardiac parameters in SHR prior to MI. Fractional shortening (FS) was decreased to 18.4 ± 1.0% in vehicle-treated MI rats compared with corresponding sham (30.6 ± 1.0%) 7 weeks following MI induction. In infarcted SHR hearts, EET-B treatment improved FS (23.7 ± 0.7%), markedly increased heme oxygenase-1 (HO-1) immunopositivity in cardiomyocytes and reduced cardiac inflammation and fibrosis (by 13 and 19%, respectively). In conclusion, these findings suggest that EET analog EET-B has beneficial therapeutic actions to reduce cardiac remodeling in SHR subjected to MI.
650    _2
$a zvířata $7 D000818
650    _2
$a kyseliny arachidonové $x aplikace a dávkování $x chemie $7 D001095
650    _2
$a krevní tlak $7 D001794
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a srdce $x patofyziologie $7 D006321
650    _2
$a hemoxygenasa-1 $x genetika $x metabolismus $7 D051547
650    _2
$a lidé $7 D006801
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a infarkt myokardu $x farmakoterapie $x genetika $x metabolismus $x patofyziologie $7 D009203
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani inbrední SHR $7 D011918
655    _2
$a časopisecké články $7 D016428
655    _2
$a Research Support, N.I.H., Extramural $7 D052061
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Hye Khan, Md Abdul $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, U.S.A.
700    1_
$a Gross, Garrett J $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, U.S.A.
700    1_
$a Cyprová, Michaela $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Hrdlička, Jaroslav $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Kvasilová, Alena $u Institute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
700    1_
$a Falck, John R $u Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, U.S.A.
700    1_
$a Campbell, William B $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, U.S.A.
700    1_
$a Sedláková, Lenka, $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. $d 1992- $7 xx0273377
700    1_
$a Škutová, Šárka $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Olejníčková, Veronika, $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. Institute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic. $d 1986- $7 mub2015894084
700    1_
$a Gregorovičová, Martina $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Sedmera, David $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic. Institute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic.
700    1_
$a Kolář, František $u Department of Developmental Cardiology, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Imig, John D $u Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, U.S.A.
773    0_
$w MED00009494 $t Clinical science (London, England : 1979) $x 1470-8736 $g Roč. 133, č. 8 (2019), s. 939-951
856    41
$u https://pubmed.ncbi.nlm.nih.gov/30979784 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20200511 $b ABA008
991    __
$a 20220530145434 $b ABA008
999    __
$a ok $b bmc $g 1525321 $s 1096519
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2019 $b 133 $c 8 $d 939-951 $e 20190429 $i 1470-8736 $m Clinical science (1979) $n Clin Sci (Lond) $x MED00009494
GRA    __
$a R01 DK103616 $p NIDDK NIH HHS $2 United States
GRA    __
$a R01 HL111392 $p NHLBI NIH HHS $2 United States
GRA    __
$a R01 HL132908 $p NHLBI NIH HHS $2 United States
GRA    __
$a NV15-27735A $p MZ0
LZP    __
$a Pubmed-20200511

Find record

Citation metrics

Loading data ...

Archiving options

Loading data ...