Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-4-29
pubmed:abstractText
Reactive oxygen species (ROS) participate in cardioprotection of ischemic reperfusion (I/R) injury via preconditioning mechanisms. Mitochondrial ROS have been shown to play a key role in this process. Angiotensin II (Ang II) exhibits pharmacological preconditioning; however, the involvement of NAD(P)H oxidase, known as an ROS-generating enzyme responsive to Ang II stimuli, in the preconditioning process remains unclear. We compared the effects of 5-hydroxydecanoate (5-HD; an inhibitor of mitochondrial ATP-sensitive potassium channels), apocynin (an NAD(P)H oxidase inhibitor), and 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (tempol; a membrane permeable radical scavenger) on pharmacological preconditioning by Ang II in rat cardiac I/R injury in vivo. Treatment with a pressor dose of Ang II before a 30-minute coronary occlusion reduced infarct size as determined 24 hours after reperfusion. The protective effects of Ang II were eliminated by pretreatment with 5-HD or apocynin, similar to tempol. Both 5-HD and apocynin suppressed the enhanced cardiac lipid peroxidation and activation of the apoptosis signal-regulating kinase/p38, c-Jun NH2-terminal kinase (JNK) pathways, but not the Raf/MEK/extracellular signal-regulated kinase pathway, elicited by acutely administered Ang II. Apocynin but not 5-HD suppressed Ang II-induced augmentations of the NAD(P)H oxidase complex formation (p47phox, p22phox, and Rac-1) and its activity in the heart. Finally, 5-HD suppressed superoxide production by isolated cardiac mitochondria without any effect on their respiration. These results suggest that the preconditioning effects of Ang II for cardiac I/R injury may be mediated by cardiac mitochondria-derived ROS enhanced through NAD(P)H oxidase via JNK and p38 mitogen-activated protein kinase activation.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/5-hydroxydecanoic acid, http://linkedlifedata.com/resource/pubmed/chemical/Acetophenones, http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II, http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Decanoic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxy Acids, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase, http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species, http://linkedlifedata.com/resource/pubmed/chemical/Superoxides, http://linkedlifedata.com/resource/pubmed/chemical/acetovanillone
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
860-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15824196-Acetophenones, pubmed-meshheading:15824196-Angiotensin II, pubmed-meshheading:15824196-Animals, pubmed-meshheading:15824196-Cardiotonic Agents, pubmed-meshheading:15824196-Decanoic Acids, pubmed-meshheading:15824196-Enzyme Activation, pubmed-meshheading:15824196-Enzyme Inhibitors, pubmed-meshheading:15824196-Hydroxy Acids, pubmed-meshheading:15824196-Ischemic Preconditioning, Myocardial, pubmed-meshheading:15824196-Lipid Peroxidation, pubmed-meshheading:15824196-Mitochondria, pubmed-meshheading:15824196-Mitogen-Activated Protein Kinases, pubmed-meshheading:15824196-Myocardial Reperfusion Injury, pubmed-meshheading:15824196-Myocardium, pubmed-meshheading:15824196-NADPH Oxidase, pubmed-meshheading:15824196-Phagocytes, pubmed-meshheading:15824196-Rats, pubmed-meshheading:15824196-Reactive Oxygen Species, pubmed-meshheading:15824196-Superoxides
pubmed:year
2005
pubmed:articleTitle
Role of NAD(P)H oxidase- and mitochondria-derived reactive oxygen species in cardioprotection of ischemic reperfusion injury by angiotensin II.
pubmed:affiliation
Department of Pharmacology, Kagawa University Medical School, Miki, Kagawa, Japan. kimura@kms.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't