PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species.
Identifieur interne : 000331 ( Main/Exploration ); précédent : 000330; suivant : 000332PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species.
Auteurs : Jihwa Kim [Corée du Sud] ; Jooyeon Kim [Corée du Sud] ; Hyun Kook [Corée du Sud] ; Woo Jin Park [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2017.
Descripteurs français
- KwdFr :
- Angiotensine-II (pharmacologie), Animaux (MeSH), Cellules cultivées (MeSH), Espace intracellulaire (effets des médicaments et des substances chimiques), Espace intracellulaire (métabolisme), Espèces réactives de l'oxygène (métabolisme), Fer (métabolisme), Lésion de reperfusion myocardique (génétique), Lésion de reperfusion myocardique (métabolisme), Microscopie de fluorescence (MeSH), Myocytes cardiaques (cytologie), Myocytes cardiaques (effets des médicaments et des substances chimiques), Myocytes cardiaques (métabolisme), Mâle (MeSH), Oxydants (pharmacologie), Peroxyde d'hydrogène (pharmacologie), Protein-disulfide reductase (glutathione) (MeSH), Protéines de transport (génétique), Protéines de transport (métabolisme), Relation dose-effet des médicaments (MeSH), Souris knockout (MeSH), Souris transgéniques (MeSH), Survie cellulaire (effets des médicaments et des substances chimiques), Survie cellulaire (génétique).
- MESH :
- cytologie : Myocytes cardiaques.
- effets des médicaments et des substances chimiques : Espace intracellulaire, Myocytes cardiaques, Survie cellulaire.
- génétique : Lésion de reperfusion myocardique, Protéines de transport, Survie cellulaire.
- métabolisme : Espace intracellulaire, Espèces réactives de l'oxygène, Fer, Lésion de reperfusion myocardique, Myocytes cardiaques, Protéines de transport.
- pharmacologie : Angiotensine-II, Oxydants, Peroxyde d'hydrogène.
- Animaux, Cellules cultivées, Microscopie de fluorescence, Mâle, Protein-disulfide reductase (glutathione), Relation dose-effet des médicaments, Souris knockout, Souris transgéniques.
English descriptors
- KwdEn :
- Angiotensin II (pharmacology), Animals (MeSH), Carrier Proteins (genetics), Carrier Proteins (metabolism), Cell Survival (drug effects), Cell Survival (genetics), Cells, Cultured (MeSH), Dose-Response Relationship, Drug (MeSH), Hydrogen Peroxide (pharmacology), Intracellular Space (drug effects), Intracellular Space (metabolism), Iron (metabolism), Male (MeSH), Mice, Knockout (MeSH), Mice, Transgenic (MeSH), Microscopy, Fluorescence (MeSH), Myocardial Reperfusion Injury (genetics), Myocardial Reperfusion Injury (metabolism), Myocytes, Cardiac (cytology), Myocytes, Cardiac (drug effects), Myocytes, Cardiac (metabolism), Oxidants (pharmacology), Protein Disulfide Reductase (Glutathione) (MeSH), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , genetics : Carrier Proteins.
- chemical , metabolism : Carrier Proteins, Iron, Reactive Oxygen Species.
- chemical , pharmacology : Angiotensin II, Hydrogen Peroxide, Oxidants.
- cytology : Myocytes, Cardiac.
- drug effects : Cell Survival, Intracellular Space, Myocytes, Cardiac.
- genetics : Cell Survival, Myocardial Reperfusion Injury.
- metabolism : Intracellular Space, Myocardial Reperfusion Injury, Myocytes, Cardiac.
- Animals, Cells, Cultured, Dose-Response Relationship, Drug, Male, Mice, Knockout, Mice, Transgenic, Microscopy, Fluorescence, Protein Disulfide Reductase (Glutathione).
Abstract
Excessive generation of reactive oxygen species (ROS) is one of the main causes of myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the role of protein kinase C-interacting cousin of thioredoxin (PICOT; Grx3) during myocardial I/R using PICOT transgenic (TG) and knockdown (KD) mice. Infarction and apoptosis were attenuated in PICOT TG mice but exacerbated in PICOT KD mice upon I/R. In parallel, I/R-induced generation of ROS was attenuated in PICOT TG mice but exacerbated in PICOT KD mice. Angiotensin II (AngII)-mediated increases in ROS and free iron levels were also attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Accordingly, H2O2-mediated cell death was attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Taken together, these data show that PICOT alleviates myocardial I/R injury by regulating intracellular ROS and free iron levels. We suggest that PICOT presents a novel therapeutic strategy for myocardial I/R injury.
DOI: 10.1016/j.bbrc.2017.02.136
PubMed: 28257842
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Electronic address: woojinpark@icloud.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Life Sciences, Gwangju Institute of Science and Technology, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005</wicri:regionArea><wicri:noRegion>Gwangju 61005</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiotensin II (pharmacology)</term><term>Animals (MeSH)</term><term>Carrier Proteins (genetics)</term><term>Carrier Proteins (metabolism)</term><term>Cell Survival (drug effects)</term><term>Cell Survival (genetics)</term><term>Cells, Cultured (MeSH)</term><term>Dose-Response Relationship, Drug (MeSH)</term><term>Hydrogen Peroxide (pharmacology)</term><term>Intracellular Space (drug effects)</term><term>Intracellular Space (metabolism)</term><term>Iron (metabolism)</term><term>Male (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Microscopy, Fluorescence (MeSH)</term><term>Myocardial Reperfusion Injury (genetics)</term><term>Myocardial Reperfusion Injury (metabolism)</term><term>Myocytes, Cardiac (cytology)</term><term>Myocytes, Cardiac (drug effects)</term><term>Myocytes, Cardiac (metabolism)</term><term>Oxidants (pharmacology)</term><term>Protein Disulfide Reductase (Glutathione) (MeSH)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Angiotensine-II (pharmacologie)</term><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Espace intracellulaire (effets des médicaments et des substances chimiques)</term><term>Espace intracellulaire (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Fer (métabolisme)</term><term>Lésion de reperfusion myocardique (génétique)</term><term>Lésion de reperfusion myocardique (métabolisme)</term><term>Microscopie de fluorescence (MeSH)</term><term>Myocytes cardiaques (cytologie)</term><term>Myocytes cardiaques (effets des médicaments et des substances chimiques)</term><term>Myocytes cardiaques (métabolisme)</term><term>Mâle (MeSH)</term><term>Oxydants (pharmacologie)</term><term>Peroxyde d'hydrogène (pharmacologie)</term><term>Protein-disulfide reductase (glutathione) (MeSH)</term><term>Protéines de transport (génétique)</term><term>Protéines de transport (métabolisme)</term><term>Relation dose-effet des médicaments (MeSH)</term><term>Souris knockout (MeSH)</term><term>Souris transgéniques (MeSH)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Survie cellulaire (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Carrier Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Iron</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Angiotensin II</term><term>Hydrogen Peroxide</term><term>Oxidants</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Survival</term><term>Intracellular Space</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Espace intracellulaire</term><term>Myocytes cardiaques</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Survival</term><term>Myocardial Reperfusion Injury</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Lésion de reperfusion myocardique</term><term>Protéines de transport</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Intracellular Space</term><term>Myocardial Reperfusion Injury</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espace intracellulaire</term><term>Espèces réactives de l'oxygène</term><term>Fer</term><term>Lésion de reperfusion myocardique</term><term>Myocytes cardiaques</term><term>Protéines de transport</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Angiotensine-II</term><term>Oxydants</term><term>Peroxyde d'hydrogène</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Dose-Response Relationship, Drug</term><term>Male</term><term>Mice, Knockout</term><term>Mice, Transgenic</term><term>Microscopy, Fluorescence</term><term>Protein Disulfide Reductase (Glutathione)</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Microscopie de fluorescence</term><term>Mâle</term><term>Protein-disulfide reductase (glutathione)</term><term>Relation dose-effet des médicaments</term><term>Souris knockout</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Excessive generation of reactive oxygen species (ROS) is one of the main causes of myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the role of protein kinase C-interacting cousin of thioredoxin (PICOT; Grx3) during myocardial I/R using PICOT transgenic (TG) and knockdown (KD) mice. Infarction and apoptosis were attenuated in PICOT TG mice but exacerbated in PICOT KD mice upon I/R. In parallel, I/R-induced generation of ROS was attenuated in PICOT TG mice but exacerbated in PICOT KD mice. Angiotensin II (AngII)-mediated increases in ROS and free iron levels were also attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Accordingly, H<sub>2</sub>O<sub>2</sub>-mediated cell death was attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Taken together, these data show that PICOT alleviates myocardial I/R injury by regulating intracellular ROS and free iron levels. We suggest that PICOT presents a novel therapeutic strategy for myocardial I/R injury.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28257842</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>12</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>485</Volume><Issue>4</Issue><PubDate><Year>2017</Year><Month>04</Month><Day>15</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species.</ArticleTitle><Pagination><MedlinePgn>807-813</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(17)30436-9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2017.02.136</ELocationID><Abstract><AbstractText>Excessive generation of reactive oxygen species (ROS) is one of the main causes of myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the role of protein kinase C-interacting cousin of thioredoxin (PICOT; Grx3) during myocardial I/R using PICOT transgenic (TG) and knockdown (KD) mice. Infarction and apoptosis were attenuated in PICOT TG mice but exacerbated in PICOT KD mice upon I/R. In parallel, I/R-induced generation of ROS was attenuated in PICOT TG mice but exacerbated in PICOT KD mice. Angiotensin II (AngII)-mediated increases in ROS and free iron levels were also attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Accordingly, H<sub>2</sub>O<sub>2</sub>-mediated cell death was attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Taken together, these data show that PICOT alleviates myocardial I/R injury by regulating intracellular ROS and free iron levels. We suggest that PICOT presents a novel therapeutic strategy for myocardial I/R injury.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jihwa</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Life Sciences, Gwangju Institute of Science and Technology, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jooyeon</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Life Sciences, Gwangju Institute of Science and Technology, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kook</LastName><ForeName>Hyun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Medical Research Center for Gene Regulation, Chonnam National University Medical School, 160 Baekseo-ro, Dong-ku, Gwangju 61469, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Woo Jin</ForeName><Initials>WJ</Initials><AffiliationInfo><Affiliation>College of Life Sciences, Gwangju Institute of Science and Technology, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 61005, Republic of Korea. Electronic address: woojinpark@icloud.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016877">Oxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>11128-99-7</RegistryNumber><NameOfSubstance UI="D000804">Angiotensin II</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.4.2</RegistryNumber><NameOfSubstance UI="D011490">Protein Disulfide Reductase (Glutathione)</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.4.2</RegistryNumber><NameOfSubstance UI="C498606">Txnl2 protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042541" MajorTopicYN="N">Intracellular Space</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008856" MajorTopicYN="N">Microscopy, Fluorescence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016877" MajorTopicYN="N">Oxidants</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011490" MajorTopicYN="N">Protein Disulfide Reductase (Glutathione)</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Free iron</Keyword><Keyword MajorTopicYN="Y">Glutaredoxin 3</Keyword><Keyword MajorTopicYN="Y">Heart</Keyword><Keyword MajorTopicYN="Y">Ischemia-reperfusion injury</Keyword><Keyword MajorTopicYN="Y">PICOT</Keyword><Keyword MajorTopicYN="Y">ROS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>02</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>02</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>3</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28257842</ArticleId><ArticleId IdType="pii">S0006-291X(17)30436-9</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2017.02.136</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Kim, Jihwa" sort="Kim, Jihwa" uniqKey="Kim J" first="Jihwa" last="Kim">Jihwa Kim</name></noRegion><name sortKey="Kim, Jooyeon" sort="Kim, Jooyeon" uniqKey="Kim J" first="Jooyeon" last="Kim">Jooyeon Kim</name><name sortKey="Kook, Hyun" sort="Kook, Hyun" uniqKey="Kook H" first="Hyun" last="Kook">Hyun Kook</name><name sortKey="Park, Woo Jin" sort="Park, Woo Jin" uniqKey="Park W" first="Woo Jin" last="Park">Woo Jin Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species.
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