The Role of Anakinra in the Modulation of Intestinal Cell Apoptosis and Inflammatory Response During Ischemia/Reperfusion

dc.contributor.author Kandemir, Muhammed
dc.contributor.author Bektur Aykanat, Nuriye Ezgi
dc.contributor.author Yaşar, Necdet Fatih
dc.contributor.author Özkurt, Mete
dc.contributor.author Özyurt, Rumeysa
dc.contributor.author Aykanat, Nuriye Ezgi Bektur
dc.contributor.author Erkasap, Nilüfer
dc.contributor.author Bektur Aykanat, Nuriye Ezgi
dc.contributor.other Basic Sciences
dc.contributor.other Basic Sciences
dc.date.accessioned 2024-07-05T15:19:30Z
dc.date.available 2024-07-05T15:19:30Z
dc.date.issued 2021
dc.description Yasar, Necdet/0000-0002-9751-2912; OZYURT, RUMEYSA/0000-0002-9887-2645; OZKURT, METE/0000-0003-4000-2345 en_US
dc.description.abstract Background/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, anakinra en_US
dc.description.sponsorship Eskisehir Osmangazi University Scientific Research Projects Commission en_US
dc.description.sponsorship This project was supported by the Eskisehir Osmangazi University Scientific Research Projects Commission. en_US
dc.identifier.doi 10.3906/sag-2008-258
dc.identifier.issn 1300-0144
dc.identifier.issn 1303-6165
dc.identifier.scopus 2-s2.0-85114239746
dc.identifier.uri https://doi.org/10.3906/sag-2008-258
dc.identifier.uri https://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.uri https://hdl.handle.net/20.500.14411/1970
dc.language.iso en en_US
dc.publisher Tubitak Scientific & Technological Research Council Turkey en_US
dc.relation.ispartof Turkish Journal of Medical Sciences en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.title The Role of Anakinra in the Modulation of Intestinal Cell Apoptosis and Inflammatory Response During Ischemia/Reperfusion en_US
dc.type Article en_US
dspace.entity.type Publication
gdc.author.id Yasar, Necdet/0000-0002-9751-2912
gdc.author.id OZYURT, RUMEYSA/0000-0002-9887-2645
gdc.author.id OZKURT, METE/0000-0003-4000-2345
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gdc.author.wosid özkurt, mete/ACM-2771-2022
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gdc.bip.popularityclass C4
gdc.coar.access open access
gdc.coar.type text::journal::journal article
gdc.collaboration.industrial false
gdc.description.department Atılım University en_US
gdc.description.departmenttemp ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ,Tanımlanmamış Kurum,ATILIM ÜNİVERSİTESİ,ESKİŞEHİR OSMANGAZİ ÜNİVERSİTESİ en_US
gdc.description.endpage 2184 en_US
gdc.description.issue 4 en_US
gdc.description.publicationcategory Makale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı en_US
gdc.description.scopusquality Q2
gdc.description.startpage 2177 en_US
gdc.description.volume 51 en_US
gdc.description.wosquality Q3
gdc.identifier.openalex W3153331099
gdc.identifier.pmid 33843175
gdc.identifier.trdizinid 481047
gdc.identifier.wos WOS:000691664800011
gdc.index.type WoS
gdc.index.type Scopus
gdc.index.type TR-Dizin
gdc.index.type PubMed
gdc.oaire.accesstype GOLD
gdc.oaire.diamondjournal false
gdc.oaire.impulse 4.0
gdc.oaire.influence 2.6579203E-9
gdc.oaire.isgreen true
gdc.oaire.keywords Caspase 3
gdc.oaire.keywords Interleukin-6
gdc.oaire.keywords Superoxide Dismutase
gdc.oaire.keywords Tumor Necrosis Factor-alpha
gdc.oaire.keywords Apoptosis
gdc.oaire.keywords Article
gdc.oaire.keywords Rats
gdc.oaire.keywords Interleukin 1 Receptor Antagonist Protein
gdc.oaire.keywords Ischemia
gdc.oaire.keywords Antirheumatic Agents
gdc.oaire.keywords Malondialdehyde
gdc.oaire.keywords Reperfusion Injury
gdc.oaire.keywords Reperfusion
gdc.oaire.keywords Animals
gdc.oaire.popularity 5.318193E-9
gdc.oaire.publicfunded false
gdc.oaire.sciencefields 0301 basic medicine
gdc.oaire.sciencefields 03 medical and health sciences
gdc.oaire.sciencefields 0302 clinical medicine
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gdc.opencitations.count 4
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gdc.scopus.citedcount 6
gdc.virtual.author Bektur Aykanat, Nuriye Ezgi
gdc.wos.citedcount 6
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