Melatonin protects myocardium from ischemia-reperfusion injury in hypertensive rats: Role of myeloperoxidase activity

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dc.authoridbay karabulut, aysun/0000-0002-7873-2805
dc.authoridBurma, Oktay/0000-0002-0880-4578
dc.authorwosidbay karabulut, aysun/HJP-0995-2023
dc.authorwosidBurma, Oktay/W-4151-2018
dc.contributor.authorSahna, Engin
dc.contributor.authorDeniz, Esra
dc.contributor.authorBay-Karabulut, Aysun
dc.contributor.authorBurma, Oktay
dc.date.accessioned2024-08-04T20:31:00Z
dc.date.available2024-08-04T20:31:00Z
dc.date.issued2008
dc.departmentİnönü Üniversitesien_US
dc.description.abstractIncreased levels of reactive oxygen species, alterations in nitric oxide synthesis, and increased migration of neutrophils to the ischemic tissue play an important role in the pathophysiology of myocardial ischemia-reperfusion (IR) injury. In this study, we have evaluated the effects of melatonin on myeloperoxidase (MPO) activity, tissue glutathione (GSH), lipid peroxidation levels, and blood pressure in L-NAME-induced hypertensive rats with or without IR. NOS inhibitor L-NAME was administrated before inducing cardiac ischemia for 15 days intraperitoneally. For the cardiac ischemia, the left coronary artery was ligated for 30 min, and reperfusion was performed for 120 min after the ischemia. L-NAME treatment in non-ischemic animals increased blood pressure and lipid peroxidation, and decreased glutathione level in myocardial tissue significantly as compared with non-L-NAME-treated animals. Melatonin reversed L-NAME-induced blood pressure elevation and oxidative changes. Cardiac IR increased MDA levels and MPO activity and decreased GSH levels as compared with non-ischemic animals. L-NAME treatment did not change in IR-induced MDA and GSH levels as compared with ischemic control animals. However, MPO activity was significantly higher than control ischemic animals. MDA levels and MPO activity resulting from ischemic injury in melatonin-treated animals were significantly less than L-NAME-treated animals. Taken togetherthe ischemic and non-ischemic control and melatonin-treated animalsthis study shows that neutrophil migration plays an important role on the development of ischemic injury in hypertensive rats.en_US
dc.identifier.doi10.1080/10641960802251966
dc.identifier.endpage681en_US
dc.identifier.issn1064-1963
dc.identifier.issn1525-6006
dc.identifier.issue7en_US
dc.identifier.pmid18855270en_US
dc.identifier.scopus2-s2.0-54049124483en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage673en_US
dc.identifier.urihttps://doi.org/10.1080/10641960802251966
dc.identifier.urihttps://hdl.handle.net/11616/94669
dc.identifier.volume30en_US
dc.identifier.wosWOS:000260035100019en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofClinical and Experimental Hypertensionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectNOen_US
dc.subjecthypertensionen_US
dc.subjectmelatoninen_US
dc.subjectischemia-reperfusionen_US
dc.subjectmyeloperoxidaseen_US
dc.subjecthearten_US
dc.titleMelatonin protects myocardium from ischemia-reperfusion injury in hypertensive rats: Role of myeloperoxidase activityen_US
dc.typeArticleen_US

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