Source:http://linkedlifedata.com/resource/pubmed/id/15824196
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2005-4-29
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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.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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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
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1524-4563
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
45
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
860-6
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pubmed:dateRevised |
2009-11-19
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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
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pubmed:year |
2005
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pubmed:articleTitle |
Role of NAD(P)H oxidase- and mitochondria-derived reactive oxygen species in cardioprotection of ischemic reperfusion injury by angiotensin II.
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pubmed:affiliation |
Department of Pharmacology, Kagawa University Medical School, Miki, Kagawa, Japan. kimura@kms.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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