© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
COX-2: an in vivo evidence of its participation in heat stress-induced myocardial preconditioning
Laboratoire Hypoxie Physio-Pathologie, Facultés de Pharmacie, Domaine de la Merci, La Tronche, France
christophe.ribuot{at}ujf-grenoble.fr
* Corresponding author. Laboratoire Stress Cardiovasculaire et Pathologies Associées, Faculté de Pharmacie, Domaine de la Merci, 38706 La Tronche, France. Tel.: +33-4-7663-7108; fax: +33-4-7663-7152.
Objective: Heat stress (HS) is known to induce delayed protection against myocardial infarction. We have previously shown that inducible nitric oxide synthase (iNOS), was involved in mediating this form of preconditioning. Since iNOS and cyclooxygenase-2 (COX-2) are co-induced in various cell types, the goal of this study was to investigate whether COX-2 could also participate to the HS-induced cardioprotection. Methods and Results: A total of 78 male Wistar rats, subjected to either heat stress (42°C for 15 min) or sham anaesthesia were used for this study. Twenty-four hours later, they were treated or not with a selective COX-2 inhibitor, either celecoxib (3 mg kg–1, i.p.) or NS-398 (5 mg kg–1, i.p.), 30 min before being subjected to a 30-min occlusion of the left coronary artery followed by a 120-min reperfusion, in vivo. HS resulted in a marked increase in myocardial COX-2 protein expression at 24 h, associated with a significant protection against infarction (46.0±1.4% in sham vs. 26.8±3.8% in HS group) (P
0.05). Administration of selective COX-2 inhibitor 24 h after HS, completely abrogated this delayed cardioprotection (46.4±3.6 and 48.0±2.8%, respectively, in HS+celecoxib and HS+NS-398 groups). Conclusion: This study provides the first evidence of an implication of COX-2 as a mediator of HS-induced cardioprotection. This suggests that prostaglandins are involved in this type of cardioprotective preconditioning.
KEYWORDS COX-2, cyclooxygenase-2; HR, heart rate; HS, heat stress; Hsp, heat shock protein; I, infarct zone; IL-1β, interleukin-1β; iNOS inducible nitric oxide synthase; IP, ischaemic preconditioning; LCA, left coronary artery; LV, left ventricle; MAP, mean arterial pressure; MAPK, mitogen activated protein kinase; NF-
B, nuclear factor-kappa B; PGs, prostaglandins; PKC, protein kinase C; R, risk zone; ROS, reactive oxygen species; TNF-
, tumour necrosis factor-
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  H. Sato, R. Bolli, G. D. Rokosh, Q. Bi, S. Dai, G. Shirk, and X.-L. Tang The cardioprotection of the late phase of ischemic preconditioning is enhanced by postconditioning via a COX-2-mediated mechanism in conscious rats Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2557 - H2564. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Jiang, E. Shi, Y. Nakajima, S. Sato, K. Ohno, and H. Yue Cyclooxygenase-1 Mediates the Final Stage of Morphine-Induced Delayed Cardioprotection in Concert With Cyclooxygenase-2 J. Am. Coll. Cardiol., May 17, 2005; 45(10): 1707 - 1715. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Joyeux-Faure, C. Arnaud, D. Godin-Ribuot, and C. Ribuot Heat stress preconditioning and delayed myocardial protection: what is new? Cardiovasc Res, December 1, 2003; 60(3): 469 - 477. [Abstract] [Full Text] [PDF]
|
|