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Aydemir-Koksoy, Aslihan; Bilginoglu, Ayca; Sariahmetoglu, Meltem; Schulz, Richard; Turan, Belma
<?xml version='1.0' encoding='utf-8'?> <resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd"> <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/25205</identifier> <creators> <creator> <creatorName>Aydemir-Koksoy, Aslihan</creatorName> <givenName>Aslihan</givenName> <familyName>Aydemir-Koksoy</familyName> <affiliation>Ankara Univ, Dept Biophys, Fac Med, TR-06100 Ankara, Turkey</affiliation> </creator> <creator> <creatorName>Bilginoglu, Ayca</creatorName> <givenName>Ayca</givenName> <familyName>Bilginoglu</familyName> <affiliation>Ankara Univ, Dept Biophys, Fac Med, TR-06100 Ankara, Turkey</affiliation> </creator> <creator> <creatorName>Sariahmetoglu, Meltem</creatorName> <givenName>Meltem</givenName> <familyName>Sariahmetoglu</familyName> </creator> <creator> <creatorName>Schulz, Richard</creatorName> <givenName>Richard</givenName> <familyName>Schulz</familyName> </creator> <creator> <creatorName>Turan, Belma</creatorName> <givenName>Belma</givenName> <familyName>Turan</familyName> <affiliation>Ankara Univ, Dept Biophys, Fac Med, TR-06100 Ankara, Turkey</affiliation> </creator> </creators> <titles> <title>Antioxidant Treatment Protects Diabetic Rats From Cardiac Dysfunction By Preserving Contractile Protein Targets Of Oxidative Stress</title> </titles> <publisher>Aperta</publisher> <publicationYear>2010</publicationYear> <dates> <date dateType="Issued">2010-01-01</date> </dates> <resourceType resourceTypeGeneral="Text">Journal article</resourceType> <alternateIdentifiers> <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/25205</alternateIdentifier> </alternateIdentifiers> <relatedIdentifiers> <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1016/j.jnutbio.2009.06.006</relatedIdentifier> </relatedIdentifiers> <rightsList> <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights> <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights> </rightsList> <descriptions> <description descriptionType="Abstract">Backgound Animal studies suggest that reactive oxygen species (ROS) play an important role in the development of diabetic cardiomyopathy. Hypothesis. Matrix metalloproteinase-2 (MMP-2) is activated by ROS and contributes to the acute loss of myocardial contractile function by targeting and cleaving susceptible proteins including troponin I (Inc) and alpha-actinin. Methods Using the streptozotocin-induced diabetic rat model, we evaluated the effect of daily in vivo administration of sodium selenate (0 3 mg/kg; DMS group), or a pure omega-3 fish oil with antioxidant vitamin E (omega-3E, 50 mg/kg. DMFA group), which has antioxidant-like effects, for 4 weeks on heart function and on several biochemical parameters related to oxidant stress and MMP-2. Results. Although both treatments prevented the diabetes-induced depression in left ventricular developed pressure (LVDP) as well as the rates of changes in developed pressure (+/-dP/dt) (P&lt;.001), the improvement in LVDP of the DMS group was greater compared to that of the DMFA group (P&lt;.001). Moreover, these treatments reduced the diabetes-induced increase in myocardial oxidized protein sulfhydryl and nitrite concentrations (P&lt;.001). Gelatin zymography and Western blot data indicated that the diabetes-induced changes in myocardial levels of MMP-2 and tissue inhibitor of matrix metalloproteinase-4 (TIMP-4) and the reduction in TnI and alpha-actinin protein levels were improved in both the DMS and DMFA groups (P&lt;.001). Conclusions: These results suggest that diabetes-induced alterations in MMP-2 and TIMP-4 contribute to myocardial contractile dysfunction by targeting TnI and alpha-actinin and that sodium selenate or omega-3E could have therapeutic benefits in diabetic cardiomyopathy. (C) 2010 Elsevier Inc. All rights reserved.</description> </descriptions> </resource>
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