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dc.contributor.authorKurt, Aysel
dc.contributor.authorTümkaya, Levent
dc.contributor.authorKalkan, Yıldıray
dc.contributor.authorTürüt, Hasan
dc.contributor.authorCüre, Medine Cumhur
dc.contributor.authorCüre, Erkan
dc.contributor.authorŞehitoğlu, İbrahim
dc.contributor.authorBilgin, Hacer
dc.contributor.authorUsta, Mustafa
dc.date.accessioned2020-12-19T20:17:09Z
dc.date.available2020-12-19T20:17:09Z
dc.date.issued2015
dc.identifier.citationKurt, A., Tumkaya, L., Kalkan, Y., Turut, H., Cure, M. C., Cure, E., Sehitoglu, I., Bilgin, H., & Usta, M. (2015). Is adalimumab protective in ischemia-reperfusion injury in lung?. Iranian journal of basic medical sciences, 18(11), 1093–1099.en_US
dc.identifier.issn2008-3866
dc.identifier.urihttps://hdl.handle.net/11436/4341
dc.description.abstractObjective(s): Increasing cytokines and reactive oxygen species (ROS) during ischemia reperfusion (I?R) leads to the lung damage. Adalimumab (Ada) is a potent tumor necrosis factor?alpha (TNF??) inhibitor agent. We aimed to evaluate whether Ada would prevent the lung tissue from damage development over the I?R process. Materials and Methods: Twenty seven Wistar albino male rats were divided into three groups (each group had 9 rats). To the control group, only laparotomy procedure was carried out. For I?R group, first infrarenal abdominal aorta was cross?clamped during 2 hr, and then reperfusion was performed for 2 hr. To I?R+Ada group, first a single dose of 50 mg/kg Ada was given intraperitoneally and 5 days later, same I?R procedure was carried out. Results: Levels of TNF??, malondialdehyde (MDA), myeloperoxidase (MPO), endothelin?1 (ET?1) and caspase?3 enzyme activity of I?R group were higher than that of both I?R+ Ada [TNF?? (P=0.021), MDA (P=0.029), MPO (P=0.012), ET?1 (P=0.036, caspase?3 (P=0.007), respectively] and control group [TNF?? (P=0.008), MDA (P<0.001), MPO (P=0.001), ET?1 (P<0.001), caspase?3 (P<0.001), respectively]. In IR group, severe damage was detected by hematoxylin?eosin staining. This damage was found less severe in Ada treatment group. Conclusion: The release of cytokines and ET?1 in a large proportion after I?R injury, and generating of ROS in excessive quantity could cause severe damage in the lung tissue. Ada could be considered as a protective agent for lung tissue during I?R process. © 2015, Mashhad University of Medical Sciences. All rights reserved.en_US
dc.language.isoengen_US
dc.publisherMashhad University of Medical Sciencesen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAdalimumaben_US
dc.subjectEndothelin?1en_US
dc.subjectIschemia reperfusionen_US
dc.subjectLung injuryen_US
dc.subjectTumor necrosis factoralphaen_US
dc.titleIs adalimumab protective in ischemia‐reperfusion injury in lung?en_US
dc.typearticleen_US
dc.contributor.departmentRTEÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.contributor.institutionauthorKurt, Aysel
dc.contributor.institutionauthorTümkaya, Levent
dc.contributor.institutionauthorKalkan, Yıldıray
dc.contributor.institutionauthorTürüt, Hasan
dc.contributor.institutionauthorCüre, Medine Cumhur
dc.contributor.institutionauthorCüre, Erkan
dc.contributor.institutionauthorŞehitoğlu, İbrahim
dc.contributor.institutionauthorBilgin, Hacer
dc.contributor.institutionauthorUsta, Mustafa
dc.identifier.volume18en_US
dc.identifier.issue11en_US
dc.identifier.startpage1093en_US
dc.identifier.endpage1099en_US
dc.relation.journalIranian Journal of Basic Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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