The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion

dc.authoridYasar, Necdet/0000-0002-9751-2912
dc.authoridOZYURT, RUMEYSA/0000-0002-9887-2645
dc.authoridOZKURT, METE/0000-0003-4000-2345
dc.authorscopusid57245894100
dc.authorscopusid55968993500
dc.authorscopusid36768783800
dc.authorscopusid57131157500
dc.authorscopusid57008316500
dc.authorscopusid6602629843
dc.authorwosidözkurt, mete/ACM-2771-2022
dc.contributor.authorBektur Aykanat, Nuriye Ezgi
dc.contributor.authorYaşar, Necdet Fatih
dc.contributor.authorÖzkurt, Mete
dc.contributor.authorÖzyurt, Rumeysa
dc.contributor.authorAykanat, Nuriye Ezgi Bektur
dc.contributor.authorErkasap, Nilüfer
dc.contributor.otherBasic Sciences
dc.date.accessioned2024-07-05T15:19:30Z
dc.date.available2024-07-05T15:19:30Z
dc.date.issued2021
dc.departmentAtılım Universityen_US
dc.department-tempESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,Tanımlanmamış Kurum,ATILIM ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİen_US
dc.descriptionYasar, Necdet/0000-0002-9751-2912; OZYURT, RUMEYSA/0000-0002-9887-2645; OZKURT, METE/0000-0003-4000-2345en_US
dc.description.abstractBackground/aim: Even though interleukin-1 receptor antagonist, IL-1Ra, is used in certain inflammatory diseases, its effect on ischemia-reperfusion injury is a current research topic. We aimed to investigate the protective effects of anakinra, an IL-1Ra, on the I/R induced intestinal injury. Materials and methods: The rat model of intestinal ischemia-reperfusion was induced. Rats were randomized into 4 groups: (group 1) control group, (group 2) I/R group, (group 3 and 4) treatment groups (50 mg/kg and 100 mg/kg, respectively). Gene expressions of caspase-3, TNF-α, IL-1α, IL-6, and apoptotic cells in tissue samples were evaluated by PCR and TUNEL methods, respectively. Plasma levels of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were studied by the ELISA method and tissue samples were examined histopathologically as well. Results: Anakinra inhibited the expression of IL-1α, IL-6, and TNF-α and decreased the SOD, CAT, and MDA caused by ischemiareperfusion injury in both treatment groups. Caspase-3 expression and TUNEL-positive cell number in treatment groups were also less. Histopathologically, anakinra better preserved the villous structure of the small intestine at a dose of 100 mg/kg than 50 mg/kg.Conclusion: Anakinra decreased the intestinal damage caused by ischemia-reperfusion and a dose of 100 mg/kg was found to be histopathologically more effective.Key words: Ischemia reperfusion injury, interleukin-1 receptor antagonist, anakinraen_US
dc.description.sponsorshipEskisehir Osmangazi University Scientific Research Projects Commissionen_US
dc.description.sponsorshipThis project was supported by the Eskisehir Osmangazi University Scientific Research Projects Commission.en_US
dc.identifier.citation0
dc.identifier.doi10.3906/sag-2008-258
dc.identifier.endpage2184en_US
dc.identifier.issn1300-0144
dc.identifier.issn1303-6165
dc.identifier.issue4en_US
dc.identifier.pmid33843175
dc.identifier.scopus2-s2.0-85114239746
dc.identifier.scopusqualityQ1
dc.identifier.startpage2177en_US
dc.identifier.trdizinid481047
dc.identifier.urihttps://doi.org/10.3906/sag-2008-258
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/481047/the-role-of-anakinra-in-the-modulation-of-intestinal-cell-apoptosis-and-inflammatory-response-during-ischemiareperfusion
dc.identifier.volume51en_US
dc.identifier.wosWOS:000691664800011
dc.identifier.wosqualityQ3
dc.language.isoenen_US
dc.publisherTubitak Scientific & Technological Research Council Turkeyen_US
dc.relation.ispartofTurkish Journal of Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleThe role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusionen_US
dc.typeArticleen_US
dspace.entity.typePublication
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