Linked Life Data

16580698

Source:http://linkedlifedata.com/resource/pubmed/id/16580698

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25
pubmed:dateCreated
2006-5-8
pubmed:abstractText
Excessive beta-adrenergic stimulation causes cardiac toxicity, which also contributes to cardiac oxidative stress. Although uncoupling protein 2 (UCP2), a member of the mitochondrial inner membrane carrier family, can regulate energy efficiency and oxidative stress in mitochondria, little data exist regarding interactions between UCP2 expression and beta-adrenergic stimulation induced cardiac oxidative damage. We investigated whether chronic beta-adrenergic stimulation induces myocardial energy metabolism abnormality via oxidative stress, including any role of UCP2. We also examined whether 3-methyl-1-phenyl-2-pyrazolin-5-one (MIC-186; edaravone), a potent free radical scavenger, has cardioprotective effects against beta-adrenergic stimulation. Male Sprague-Dawley rats received isoproterenol (1.2 mg/kg/day) subcutaneously or/and edaravone (30 mg/kg/day) orally. Isoproterenol increased the heart/body weight ratio, accompanied by an increase in the level of myocardial thiobarbituric acid reactive substances (TBARS) and a decreased phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. Isoproterenol also markedly increased expressions of UCP2 mRNA (1.74 fold vs. non-isoproterenol) and protein (1.93 fold vs. non-isoproterenol). Edaravone had no apparent effect in hypertrophic responses, but significantly prevented both increases in TBARS and decreases in the PCr/ATP ratio. Edaravone also prevented increases in UCP2 mRNA (0.76 fold vs. isoproterenol) and protein (0.62 fold vs. isoproterenol) expressions against isoproterenol administration. Our results suggest that chronic beta-adrenergic stimulation induces myocardial energy inefficiency via excessive oxidative stress. The antioxidant effect of edaravone has potential to improve energy metabolism abnormalities against beta-adrenergic stimulation. Adequate regulation of UCP2 expression through artificial reduction of oxidative stress may play an important role in protection of the myocardial energy metabolism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2974-82
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16580698-Adrenergic beta-Agonists, pubmed-meshheading:16580698-Animals, pubmed-meshheading:16580698-Antioxidants, pubmed-meshheading:16580698-Antipyrine, pubmed-meshheading:16580698-Cardiotonic Agents, pubmed-meshheading:16580698-Energy Metabolism, pubmed-meshheading:16580698-Hemodynamics, pubmed-meshheading:16580698-Ion Channels, pubmed-meshheading:16580698-Lipid Peroxidation, pubmed-meshheading:16580698-Male, pubmed-meshheading:16580698-Membrane Transport Proteins, pubmed-meshheading:16580698-Mitochondria, Heart, pubmed-meshheading:16580698-Mitochondrial Proteins, pubmed-meshheading:16580698-Myocardium, pubmed-meshheading:16580698-Organ Size, pubmed-meshheading:16580698-Oxidative Stress, pubmed-meshheading:16580698-Rats, pubmed-meshheading:16580698-Rats, Sprague-Dawley
pubmed:year
2006
pubmed:articleTitle
An antioxidant treatment potentially protects myocardial energy metabolism by regulating uncoupling protein 2 expression in a chronic beta-adrenergic stimulation rat model.
pubmed:affiliation
Second Department of Internal Medicine, Kagawa University School of Medicine, Miki, Kita, Kagawa, 761-0793, Japan. mkto@med.kagawa-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't