AIMS: To study the cardioprotection of recombinant human erythropoietin (rhEPO) preconditioning (EPC) and to investigate the role and possible mechanism of cyclooxygenase (COX)-2 in the delayed phase of EPC. METHODS: In phase 1, myocardial ischaemia reperfusion (I-R) rat model was established by 30 minutes ligation of left descending coronary and three hours of reperfusion. Rats were given 0.9% saline solution or rhEPO 24 hours before I-R protocol. COX-2 selective inhibitor celecoxib was given for further investigation of the cardioprotection of EPC. At the end of I-R protocol, infarct sizes were measured and ultrastructural organisations were studied. In phase 2, myocardial COX-2 mRNA expressions and prostaglandins (PGs) contents were studied in different groups after euthanasia. RESULTS: It was found that EPC could elicit potent cardioprotection against I-R injury, shown by reduction of infarct size and improvement of ultrastructural organisation; whereas administration of celecoxib resulted in complete loss of this protection. EPC resulted in robust increase in COX-2 mRNA and PGs levels that were also abrogated by celecoxib. CONCLUSIONS: COX-2 plays an essential part in cardioprotection of the delayed phase of EPC in rats, which might be related to actions of PGE(2) or PGI(2), or both.
AIMS: To study the cardioprotection of recombinant humanerythropoietin (rhEPO) preconditioning (EPC) and to investigate the role and possible mechanism of cyclooxygenase (COX)-2 in the delayed phase of EPC. METHODS: In phase 1, myocardial ischaemia reperfusion (I-R) rat model was established by 30 minutes ligation of left descending coronary and three hours of reperfusion. Rats were given 0.9% saline solution or rhEPO 24 hours before I-R protocol. COX-2 selective inhibitor celecoxib was given for further investigation of the cardioprotection of EPC. At the end of I-R protocol, infarct sizes were measured and ultrastructural organisations were studied. In phase 2, myocardial COX-2 mRNA expressions and prostaglandins (PGs) contents were studied in different groups after euthanasia. RESULTS: It was found that EPC could elicit potent cardioprotection against I-R injury, shown by reduction of infarct size and improvement of ultrastructural organisation; whereas administration of celecoxib resulted in complete loss of this protection. EPC resulted in robust increase in COX-2 mRNA and PGs levels that were also abrogated by celecoxib. CONCLUSIONS:COX-2 plays an essential part in cardioprotection of the delayed phase of EPC in rats, which might be related to actions of PGE(2) or PGI(2), or both.
Authors: Jens Kristensen; Michael Maeng; Michael Rehling; Jette S Berg; Ulrik M Mortensen; Søren S Nielsen; Torsten T Nielsen Journal: Clin Physiol Funct Imaging Date: 2005-09 Impact factor: 2.273
Authors: Parvaneh Rafiee; Yang Shi; Jidong Su; Kirkwood A Pritchard; James S Tweddell; John E Baker Journal: Basic Res Cardiol Date: 2004-12-22 Impact factor: 17.165
Authors: M L Brines; P Ghezzi; S Keenan; D Agnello; N C de Lanerolle; C Cerami; L M Itri; A Cerami Journal: Proc Natl Acad Sci U S A Date: 2000-09-12 Impact factor: 11.205
Authors: K Shinmura; X L Tang; Y Wang; Y T Xuan; S Q Liu; H Takano; A Bhatnagar; R Bolli Journal: Proc Natl Acad Sci U S A Date: 2000-08-29 Impact factor: 11.205
Authors: Erik Lipsic; Peter van der Meer; Robert H Henning; Albert J H Suurmeijer; Kristien M Boddeus; Dirk J van Veldhuisen; Wiek H van Gilst; Regien G Schoemaker Journal: J Cardiovasc Pharmacol Date: 2004-10 Impact factor: 3.105