PittsburghV1, Main, Exploration, bibRecord, 002115

Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats

Identifieur interne : 002115 ( Main/Exploration ); précédent : 002114; suivant : 002116

Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats

Auteurs : Nelson Escobales ; Rebeca E. Nu Ez ; Sehwan Jang ; Rebecca Parodi-Rullan ; Sylvette Ayala-Pe A ; Joshua R. Sacher [États-Unis] ; Erin M. Skoda [États-Unis] ; Peter Wipf [États-Unis] ; Walter Frontera [États-Unis] ; Sabzali Javadov

Source :

Journal of molecular and cellular cardiology [ 0022-2828 ] ; 2014.

RBID : PMC:4312194

Descripteurs français

KwdFr :
- Animaux, Cardiotoniques (pharmacologie), Consommation d'oxygène, Ischémie myocardique (traitement médicamenteux), Lignée cellulaire, Mitochondries du myocarde (métabolisme), Mâle, N-oxydes cycliques (pharmacologie), Peroxyde d'hydrogène (métabolisme), Piégeurs de radicaux libres (pharmacologie), Potentiel de membrane mitochondriale, Protéines de transport de la membrane mitochondriale (métabolisme), Rats de lignée F344, Récupération fonctionnelle, Stress oxydatif, Évaluation préclinique de médicament.
MESH :
- métabolisme : Mitochondries du myocarde, Peroxyde d'hydrogène, Protéines de transport de la membrane mitochondriale.
- pharmacologie : Cardiotoniques, N-oxydes cycliques, Piégeurs de radicaux libres.
- traitement médicamenteux : Ischémie myocardique.
- Animaux, Consommation d'oxygène, Lignée cellulaire, Mâle, Potentiel de membrane mitochondriale, Rats de lignée F344, Récupération fonctionnelle, Stress oxydatif, Évaluation préclinique de médicament.

English descriptors

KwdEn :
- Animals, Cardiotonic Agents (pharmacology), Cell Line, Cyclic N-Oxides (pharmacology), Drug Evaluation, Preclinical, Free Radical Scavengers (pharmacology), Hydrogen Peroxide (metabolism), Male, Membrane Potential, Mitochondrial, Mitochondria, Heart (metabolism), Mitochondrial Membrane Transport Proteins (metabolism), Myocardial Ischemia (drug therapy), Oxidative Stress, Oxygen Consumption, Rats, Inbred F344, Recovery of Function.
MESH :
- chemical , metabolism : Hydrogen Peroxide, Mitochondrial Membrane Transport Proteins.
- chemical , pharmacology : Cardiotonic Agents, Cyclic N-Oxides, Free Radical Scavengers.
- drug therapy : Myocardial Ischemia.
- metabolism : Mitochondria, Heart.
- Animals, Cell Line, Drug Evaluation, Preclinical, Male, Membrane Potential, Mitochondrial, Oxidative Stress, Oxygen Consumption, Rats, Inbred F344, Recovery of Function.

Abstract

Mitochondria-generated reactive oxygen species (ROS) play a crucial role in the pathogenesis of aging and age-associated diseases. In this study, we evaluated the effects of XJB-5-131 (XJB), a mitochondria-targeted ROS and electron scavenger, on cardiac resistance to ischemia-reperfusion (IR)-induced oxidative stress in aged rats. Male adult (5-month old, n=17) and aged (29-month old, n=19) Fischer Brown Norway (F344/BN) rats were randomly assigned to the following groups: adult (A), adult+XJB (AX), aged (O), and aged+XJB (OX). XJB was administered 3 times per week (3 mg/kg body weight, IP) for four weeks. At the end of the treatment period, cardiac function was continuously monitored in excised hearts using the Langendorff technique for 30 min, followed by 20-min of global ischemia, and 60-min reperfusion. XJB improved post-ischemic recovery of aged hearts, as evidenced by greater left ventricular developed-pressures and rate-pressure products than the untreated, aged-matched group. The state 3 respiration rates at complexes I, II and IV of mitochondria isolated from XJB-treated aged hearts were 57% (P<0.05), 25% (P<0.05) and 28% (P<0.05), respectively, higher than controls. Ca²⁺-induced swelling, an indicator of permeability transition pore opening, was reduced in mitochondria of XJB-treated aged rats. In addition, XJB significantly attenuated the H₂O₂-induced depolarization of the mitochondrial inner membrane as well as total and mitochondrial ROS levels in cultured cardiomyocytes. This study underlines the importance of mitochondrial ROS in aging-induced cardiac dysfunction and suggests that targeting mitochondrial ROS may be an effective therapeutic approach to protect the aged heart against IR injury.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4312194

DOI: 10.1016/j.yjmcc.2014.10.009
PubMed: 25451170
PubMed Central: 4312194

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p id="P2">Mitochondria-generated reactive oxygen species (ROS) play a crucial role in the pathogenesis of aging and age-associated diseases. In this study, we evaluated the effects of XJB-5-131 (XJB), a mitochondria-targeted ROS and electron scavenger, on cardiac resistance to ischemia-reperfusion (IR)-induced oxidative stress in aged rats. Male adult (5-month old, n=17) and aged (29-month old, n=19) Fischer Brown Norway (F344/BN) rats were randomly assigned to the following groups: adult (A), adult+XJB (AX), aged (O), and aged+XJB (OX). XJB was administered 3 times per week (3 mg/kg body weight, IP) for four weeks. At the end of the treatment period, cardiac function was continuously monitored in excised hearts using the Langendorff technique for 30 min, followed by 20-min of global ischemia, and 60-min reperfusion. XJB improved post-ischemic recovery of aged hearts, as evidenced by greater left ventricular developed-pressures and rate-pressure products than the untreated, aged-matched group. The state 3 respiration rates at complexes I, II and IV of mitochondria isolated from XJB-treated aged hearts were 57% (<italic>P</italic>
<0.05), 25% (<italic>P</italic>
<0.05) and 28% (<italic>P</italic>
<0.05), respectively, higher than controls. Ca<sup>2+</sup>
-induced swelling, an indicator of permeability transition pore opening, was reduced in mitochondria of XJB-treated aged rats. In addition, XJB significantly attenuated the H<sub>2</sub>
O<sub>2</sub>
-induced depolarization of the mitochondrial inner membrane as well as total and mitochondrial ROS levels in cultured cardiomyocytes. This study underlines the importance of mitochondrial ROS in aging-induced cardiac dysfunction and suggests that targeting mitochondrial ROS may be an effective therapeutic approach to protect the aged heart against IR injury.</p>
</div>
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<country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Sacher, Joshua R" sort="Sacher, Joshua R" uniqKey="Sacher J" first="Joshua R." last="Sacher">Joshua R. Sacher</name>
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<name sortKey="Wipf, Peter" sort="Wipf, Peter" uniqKey="Wipf P" first="Peter" last="Wipf">Peter Wipf</name>
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Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats

Mitochondria-targeted ROS scavenger improves post-ischemic recovery of cardiac function and attenuates mitochondrial abnormalities in aged rats

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