Protective effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia-reperfusion-induced apoptotic cell death

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dc.authoridParlakpinar, Hakan/0000-0001-9497-3468
dc.authoridAcet, Ahmet/0000-0003-1131-1878
dc.authoridPolat, Alaadin/0000-0002-6920-3856
dc.authoridParlakpınar, Hakan/0000-0001-9497-3468
dc.authorwosidParlakpinar, Hakan/V-6637-2019
dc.authorwosidAcet, Ahmet/AAB-3273-2021
dc.authorwosidPolat, Alaadin/AAA-7171-2021
dc.authorwosidParlakpınar, Hakan/T-6517-2018
dc.contributor.authorParlakpinar, H
dc.contributor.authorSahna, E
dc.contributor.authorAcet, A
dc.contributor.authorMizrak, B
dc.contributor.authorPolat, A
dc.date.accessioned2024-08-04T20:13:45Z
dc.date.available2024-08-04T20:13:45Z
dc.date.issued2005
dc.departmentİnönü Üniversitesien_US
dc.description.abstractOcclusion of coronary artery causes cardiomyocyte dysfunction. Reperfusion relieves ischemia by providing cells with metabolites and oxygen, thereby preventing extensive tissue damage. Although reperfusion salvages the myocardium, it also initiates a series of events including myocardial apoptosis and necrosis. The common inducers of apoptosis include reactive oxygen species (ROS). Caffeic acid phenethyl ester (CAPE) is known as an antioxidative, anti-inflammatory effects, may protect myocardial ischemia-reperfusion (MI/R)-induced apoptosis. We have previously reported that CAPE reduced MI/R-induced necrosis. Therefore, this study was focused to investigate protective effect of CAPE on the distinct form of cell death; apoptosis in an in vivo rat model. To produce MI/R, a branch of the descending left coronary artery was occluded for 30 min followed by 2 h reperfusion. ECG changes, blood pressure (BP), and heart rate (HR) were measured before occlusion and continued both occlusion and reperfusion. CAPE (50 mu mol/kg) was given 10 min before ischemia via juguler vein. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the terminal deoxynucleotidyl transferase (TdT)-mediated d UTP-biotin nick and labeling (TUNEL) method. Also, cysteine aspartate specific proteinase (caspase)-3 and caspase-9 activities a universal effector of apoptosis, were determined. Trunk blood was extracted to determine the serum contents related to oxidant-antioxidant status. In hemodynamic parameters, there was no significant difference in HR or BP values among any group. CAPE administration had no a significant effect on hemodynamic parameters during ischemia or reperfusion. Control group revealed extensive TUNEL-positive cardiomyocytes especially in free wall of left ventricule, interventiculare septum and nearly apex zone. Intensity of TUNEL-positive cardiomyocytes reduced as a result of CAPE treatment compared to control group in the same sections. Result of the caspase activities was found to correlate with TUNEL evaluation. CAPE also, ameliorated antioxidant status. We propose that CAPE acts in the heart as a potent scavenger of free radicals to prevent the apoptotic effect of I/R. Further studies are needed to elucidate the mechanisms of apoptotic death machinery. (C) 2004 Elsevier Ireland Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.tox.2004.10.017
dc.identifier.endpage14en_US
dc.identifier.issn0300-483X
dc.identifier.issue1en_US
dc.identifier.pmid15725509en_US
dc.identifier.scopus2-s2.0-13944274084en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1en_US
dc.identifier.urihttps://doi.org/10.1016/j.tox.2004.10.017
dc.identifier.urihttps://hdl.handle.net/11616/93815
dc.identifier.volume209en_US
dc.identifier.wosWOS:000227507700001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Ireland Ltden_US
dc.relation.ispartofToxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectapoptosisen_US
dc.subjectcaffeic acid phenethyl ester (CAPE)en_US
dc.subjectreactive oxygen radicalsen_US
dc.subjectraten_US
dc.titleProtective effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia-reperfusion-induced apoptotic cell deathen_US
dc.typeArticleen_US

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