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Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?
2009
Cellular Physiology and Biochemistry
Aims: Our previous studies have shown that N-n-butyl haloperidol iodide (F 2 ) can antagonize myocardial ischemia/reperfusion (I/R) injury by blocking intracellular Ca 2+ overload and suppressing Egr-1 overexpression. The present study is to investigate the relation between the reduction of Ca 2+ 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
doi:10.1159/000257497
pmid:19910692
fatcat:2uxbzqe4avdkdg5eia7tynv444