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Ischemia-reperfusion leads to depletion of glutathione content and augmentation of malondialdehyde production in the rat heart from overproduction of oxidants: can caffeic acid phenethyl ester (CAPE) protect the heart?
- Source :
-
Molecular and cellular biochemistry [Mol Cell Biochem] 2005 May; Vol. 273 (1-2), pp. 169-75. - Publication Year :
- 2005
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Abstract
- During restoration of blood flow of the ischemic heart induced by coronary occlusion, free radicals cause lipid peroxidation with myocardial injury. Lipid peroxidation end-products, such as malondialdehyde (MDA), have been used to assess oxygen free radical-mediated injury of the ischemic-reperfused (I/R) myocardium in rats. This experimental study assessed the preventive effect of caffeic acid phenthyl ester (CAPE), antioxidant, on I/R-induced lipid peroxidation in the rat heart. We are also interested in the role of CAPE on glutathione (GSH) levels, an antioxidant whose levels are influenced by oxidative stress. I/R leads to the depletion of GSH which is the major intracellular nonprotein sulphydryl and plays an important role in the maintenance of cellular proteins and lipid in their functional state and acts primarily to protect these important structures against the threat of oxidation. In addition, we also examined morphologic changes in the heart by using light microscopy. The left coronary artery was occluded for 30 min and then reperfused for 120 min more before the experiment was terminated. CAPE (50 microM kg(-1)) was administered 10 min prior to ischemia and during occlusion by infusion. At the end of the reperfusion period, rats were sacrificed, and the heart was quickly removed for biochemical determination and histopathological analysis. I/R was accompanied by a significant increase in MDA production and decrease in GSH content in the rat heart. Administration of CAPE reduced MDA production and prevented depletion of GSH content. These beneficial changes in these biochemical parameters were also associated with parallel changes in histopathological appearance. These findings imply that I/R plays a causal role in heart injury due to overproduction of oxygen radicals or insufficient antioxidant and CAPE exert cardioprotective effects probably by the radical scavenging and antioxidant activities.
- Subjects :
- Animals
Antioxidants therapeutic use
Cardiotonic Agents pharmacology
Cardiotonic Agents therapeutic use
Free Radicals metabolism
Lipid Peroxidation drug effects
Male
Myocardial Ischemia metabolism
Myocardial Reperfusion Injury prevention & control
Myocytes, Cardiac drug effects
Myocytes, Cardiac metabolism
NF-kappa B antagonists & inhibitors
Oxidative Stress
Oxygen metabolism
Phenylethyl Alcohol pharmacology
Rats
Rats, Wistar
Antioxidants pharmacology
Caffeic Acids pharmacology
Glutathione metabolism
Heart drug effects
Malondialdehyde metabolism
Myocardial Ischemia prevention & control
Myocardial Reperfusion Injury metabolism
Phenylethyl Alcohol analogs & derivatives
Subjects
Details
- Language :
- English
- ISSN :
- 0300-8177
- Volume :
- 273
- Issue :
- 1-2
- Database :
- MEDLINE
- Journal :
- Molecular and cellular biochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 16013452
- Full Text :
- https://doi.org/10.1007/s11010-005-0551-8