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- Title
Effects of N-n-butyl Haloperidol Iodide on Myocardial Ischemia/Reperfusion Injury and Egr-1 Expression in Rat.
- Authors
Yan-Mei Zhang; Gang-Gang Shi; Zhao Tang; Jin-Hong Zheng; Wei-Qiu Li; Fu-Xiao Guo; Qiang-Yong Jia
- Abstract
We have previously shown that N-n-butyl haloperidol iodide (F2) derived from haloperidol reduces ischemia/reperfusion-induced myocardial injury by blocking intracellular Ca2+ overload. This study tested the hypothesis that cardio-protection with F2 is associated with an attenuation in the expression of early growth response gene 1 (Egr-1). In an in vivo rat model of 60 min coronary occlusion followed by 180 min of reperfusion, treatment with F2 significantly reduced myocardial injury evidenced by the reduction in release of plasma creatine kinase, myocardial creatine kinase isoenzyme and lactate dehydrogenase. In cultured neonatal rat cardiomyocytes of hypoxia for 3 h and reoxygenation for 1 h, F2 treatment attenuated necrotic and apoptotic cell death, as demonstrated by electron microscopy. Concomitant with cardio-protection by F2, the increased expression levels of Egr-1 mRNA and protein were significantly reduced in myocardial tissue and cultured cardiomyocytes as detected by reverse transcription-polymerase chain reaction, immunohistochemistry and immunocytochemistry. In conclusion, these results suggest that the protective effect of F2 on ischemia/reperfusion- or hypoxia/reoxygenation-induced myocardial injury might be partly mediated by downregulating Egr-1 expression. Edited by Ming-Hua XU
- Subjects
IODIDES; THERAPEUTICS; CORONARY disease; HEART diseases; GENE expression; CREATINE kinase; MESSENGER RNA
- Publication
Acta Biochimica et Biophysica Sinica, 2006, Vol 38, Issue 6, p435
- ISSN
1672-9145
- Publication type
Article
- DOI
10.1111/j.1745-7270.2006.00180.x