Captopril protects against burn-induced cardiopulmonary injury in rats

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dc.authorid0000-0002-0021-8400en_US
dc.contributor.authorSaglam, Esra
dc.contributor.authorSehirli, Ahmet Ozer
dc.contributor.authorOzdamar, Emine Nur
dc.contributor.authorContuk, Gazi
dc.contributor.authorCetinel, Sule
dc.contributor.authorOzsavci, Derya
dc.contributor.authorSuleymanoglu, Selami
dc.contributor.authorSener, Goksel
dc.date.accessioned2024-07-12T21:56:52Z
dc.date.available2024-07-12T21:56:52Z
dc.date.issued2014en_US
dc.departmentMaltepe Üniversitesien_US
dc.description.abstractBACKGROUND: This study was designed to determine the possible protective effect of captopril treatment against oxidative damage in heart and lung tissues induced by burn injury. METHODS: Under ether anesthesia, the shaved dorsum of Wistar albino rats was exposed to 90 C water bath for 10 seconds. Captopril was administered intraperitoneally (10 mg/kg) after the burn injury and repeated twice daily. In the sham group, the dorsum was dipped in a 25 C water bath for 10 seconds. At the end of the 24 hours, echocardiographic recordings were performed, then animals were decapitated and heart and lung tissue samples were taken for the determination of tumor necrosis factor-alpha (TNF-alpha) as a pro-inflammatory cytokine, malondialdehyde and glutathione levels and myeloperoxidase, caspase-3, and Na+, K+-ATPase activity in addition to the histological analysis. RESULTS: Burn injury caused significant alterations in left ventricular function. In heart and lung tissues, TNF-a and malondialdehyde levels and myeloperoxidase and caspase-3 activities were found to be increased, while glutathione levels and Na+, K+-ATPase activity were decreased due to burn injury. Captopril treatment significantly elevated the reduced glutathione level and Na+, K+-ATPase activity, and decreased cytokine and malondialdehyde levels and myeloperoxidase and caspase-3 activities. CONCLUSION: Captopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage.en_US
dc.identifier.doi10.5505/tjtes.2014.96493
dc.identifier.endpage160en_US
dc.identifier.issn1306-696X
dc.identifier.issue3en_US
dc.identifier.pmid24936835en_US
dc.identifier.scopus2-s2.0-84901664875en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage151en_US
dc.identifier.urihttps://dx.doi.org/10.5505/tjtes.2014.96493
dc.identifier.urihttps://hdl.handle.net/20.500.12415/8619
dc.identifier.volume20en_US
dc.identifier.wosWOS:000337163600001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherTURKISH ASSOC TRAUMA EMERGENCY SURGERYen_US
dc.relation.ispartofULUSAL TRAVMA VE ACIL CERRAHI DERGISI-TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmzKY03925
dc.subjectCaptoprilen_US
dc.subjectcytokineen_US
dc.subjectlipid peroxidationen_US
dc.subjectmyeloperoxidaseen_US
dc.subjectthermal traumaen_US
dc.titleCaptopril protects against burn-induced cardiopulmonary injury in ratsen_US
dc.typeArticle
dspace.entity.typePublication

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