dc.contributor.author | Kurt, Aysel | |
dc.contributor.author | Tümkaya, Levent | |
dc.contributor.author | Kalkan, Yıldıray | |
dc.contributor.author | Türüt, Hasan | |
dc.contributor.author | Cüre, Medine Cumhur | |
dc.contributor.author | Cüre, Erkan | |
dc.contributor.author | Şehitoğlu, İbrahim | |
dc.contributor.author | Bilgin, Hacer | |
dc.contributor.author | Usta, Mustafa | |
dc.date.accessioned | 2020-12-19T20:17:09Z | |
dc.date.available | 2020-12-19T20:17:09Z | |
dc.date.issued | 2015 | |
dc.identifier.citation | Kurt, 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.issn | 2008-3866 | |
dc.identifier.uri | https://hdl.handle.net/11436/4341 | |
dc.description.abstract | Objective(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.iso | eng | en_US |
dc.publisher | Mashhad University of Medical Sciences | en_US |
dc.rights | info:eu-repo/semantics/openAccess | en_US |
dc.subject | Adalimumab | en_US |
dc.subject | Endothelin?1 | en_US |
dc.subject | Ischemia reperfusion | en_US |
dc.subject | Lung injury | en_US |
dc.subject | Tumor necrosis factoralpha | en_US |
dc.title | Is adalimumab protective in ischemia‐reperfusion injury in lung? | en_US |
dc.type | article | en_US |
dc.contributor.department | RTEÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümü | en_US |
dc.contributor.institutionauthor | Kurt, Aysel | |
dc.contributor.institutionauthor | Tümkaya, Levent | |
dc.contributor.institutionauthor | Kalkan, Yıldıray | |
dc.contributor.institutionauthor | Türüt, Hasan | |
dc.contributor.institutionauthor | Cüre, Medine Cumhur | |
dc.contributor.institutionauthor | Cüre, Erkan | |
dc.contributor.institutionauthor | Şehitoğlu, İbrahim | |
dc.contributor.institutionauthor | Bilgin, Hacer | |
dc.contributor.institutionauthor | Usta, Mustafa | |
dc.identifier.volume | 18 | en_US |
dc.identifier.issue | 11 | en_US |
dc.identifier.startpage | 1093 | en_US |
dc.identifier.endpage | 1099 | en_US |
dc.relation.journal | Iranian Journal of Basic Medical Sciences | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |