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Table of Contents
Vol. 24, No. 5-6, 2009
Issue release date: November 2009
Section title: Original Paper
Cell Physiol Biochem 2009;24:519–526

Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Gao F.-F.1 · Jia Q.-Y.1 · Guo F.-X.1 · Zhang Y.-M.1 · Huang Z.-Q.1 · Zhou Y.-Q.1 · Chen Y.-C.1 · Shi G.-G.1,2
1Department of Pharmacology and2Department of Cardiovascular Diseases, First Affiliated Hospital, Shantou University Medical College, Shantou
email Corresponding Author

Gang-Gang Shi, Ph.D.

Department of Pharmacology, Shantou University Medical College

22 Xinling Road, Shantou, Guangdong 515041 (China)

Tel. +86-754-88900301, Fax: +86-754-88557562

E-Mail ggshi@stu.edu.cn

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Aims: Our previous studies have shown that N-n-butyl haloperidol iodide (F2) can antagonize myocardial ischemia/reperfusion (I/R) injury by blocking intracellular Ca2+ overload and suppressing Egr-1 overexpression. The present study is to investigate the relation between the reduction of Ca2+ overload and the inhibition of Egr-1 overexpression. Methods: The Sprague-Dawley rat myocardial I/R model and cultured cardiomyocyte hypoxia-reoxygenation (H/R) model were established. Administration of Egr-1 antisense oligodeoxyribonucleotide (AS-ODN) only or combining with F2, Egr-1 protein expression was examined by Western-blot analyses. Hemodynamic parameters, creatine kinase (CK) and lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA), myeloperoxidase (MPO), cardiac troponin I (cTnI), and tumor necrosis factor-α (TNF-α) were measured to assess the degree of injury and inflammation of myocardial tissues and cells. Results: Treatment with Egr-1 AS-ODN significantly reduced Egr-1 protein expression and attenuated injury and inflammation of myocardium caused by I/R or H/R evidenced by the amelioration of hemodynamics, the decrease in leakage of CK, LDH, cTnI, the increase in MDA generation, the decrease in SOD activity, the reduction of MPO activity in myocardial tissues and release of TNF-α from cultured cardiomyocytes. Treatment with F2 combined with Egr-1 AS-ODN, the inhibition of Egr-1 protein expression and inflammation (MPO activity and TNF-α level) were not enhanced, but the protection from myocardial I/R (or H/R) injury was significantly increased in hemodynamics and cytomembrane permeability relative to the using of Egr-1 AS-ODN only. Conclusion: These data suggest that the inhibition of Egr-1 overexpression cannot involve all mechanisms of cardioprotection from I/R injury.

© 2009 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: September 21, 2009
Published online: November 04, 2009
Issue release date: November 2009

Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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