Journal
LIFE SCIENCES
Volume 81, Issue 9, Pages 702-709Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2007.06.021
Keywords
apolipoprotein A-I (ApoA-I); myocardial ischemia-reperfusion injury; creatine kinase (CK); TNF-alpha; IL-6; intercellular adhesion molecule 1 (CAM-1)
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It is well established that reperfusion of heart is the optimal method for salvaging ischemic myocardium, however, the success of this therapy could be limited by reperfusion injury, which is involved in inflammatory responses. High density lipoprotein (HDL) has an anti-inflammatory function and can protect the heart from ischemia-reperfusion (I/R) injury. In this study, we investigated the cardioprotective role of apolipoprotein A-I (ApoA-I), the major apolipoprotein of HDL, in I/R injury. Using rats subjected to myocardial I/R by ligation of left anterior descending coronary artery (LAD), we found that administration of ApoA-I (20 mg/kg, iv) before the onset of reperfusion of myocardial infarction can significantly reduce serum creatine kinase (CK) levels (62.1 +/- 13.8%, p < 0.01) and heart TNF-alpha as well as IL-6 levels, compared with saline controls (40.4 +/- 14.7%, 44 +/- 9.8%, p < 0.01 respectively). Moreover, ApoA-I treatment suppresses the expression of ICAM-I on endothelium, thus diminishing neutrophil adherence, transendothelial migration, and the subsequent myocyte injury. We concluded that ApoA-I could effectively protect rat heart from I/R injury. (c) 2007 Elsevier Inc. All rights reserved.
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