Effect of anakinra, tocilizumab, and the combination thereof on bladder ischemia-reperfusion damage in albino Wistar-type rats; [Efecto de la anakinra, el tocilizumab y la combinación de ambos sobre el daño por isquemia-reperfusión vesical en ratas albinas tipo Wistar]

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Özet

Several studies have reported that oxidative stress, and proinflam-matory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-one beta (IL-1β), and interleukin-six (IL-6) are the main factors underlying bladder ischemia-reperfusion (I/R) damage. Anakinra and tocilizumab are known to be antioxidants and proinflammatory cytokine inhibitors. Our study aims to investigate if anakinra, tocilizumab, and the combination (ATC) thereof have a protective effect against oxidative and inflammatory bladder damage induced through the I/R procedure in rats, and evaluate by comparing these compounds. Male rats were divided into five groups: bladder sham-operation applied group (SG); bladder only I/R applied group (IRG); anakinra+bladder I/R applied group (AIR); tocilizumab+bladder I/R applied group (TIR); and ATC+bladder I/R applied group (ATIR). An atraumatic clamp was placed on the abdominal aorta of animals in all groups (except SG), and one hour of ischemia followed by two hours of reperfusion was performed. Our biochemical find-ings showed that anakinra and tocilizumab significantly inhibited the increase of oxidant malondialdehyde (MDA) and the decrease of antioxidants such as total glu-tathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) in bladder tissue by I/R, both at the same levels. Furthermore, anakinra and tocilizumab significantly suppressed the I/R-associated increase of TNF-α, IL-1β, and IL-6 in bladder tissue. ATC was the one that best prevented the I/R-related increase in MDA, TNF-α, IL-1β, and IL-6 and the decrease in tGSH, SOD, and CAT in the bladder tissue. ATC was more beneficial than anakinra or tocilizumab alone in treating bladder I/R damage. © 2023, Instituto de Investigaciones Clinicas. All rights reserved.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/12399Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.54817/ic.v64n3a9Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorBicer, Senol
dc.contributor.authorSuleyman, Bahadir
dc.contributor.authorMammadov, Renad
dc.contributor.authorYavuzer, Bulent
dc.contributor.authorCicek, Betul
dc.contributor.authorAltuner, Durdu
dc.contributor.authorCoban, Taha A.
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:27:18.375901979Z
dc.date.available2026-10-18T20:27:18.375901979Z
dc.date.issued2023
dc.description.abstractSeveral studies have reported that oxidative stress, and proinflam-matory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-one beta (IL-1β), and interleukin-six (IL-6) are the main factors underlying bladder ischemia-reperfusion (I/R) damage. Anakinra and tocilizumab are known to be antioxidants and proinflammatory cytokine inhibitors. Our study aims to investigate if anakinra, tocilizumab, and the combination (ATC) thereof have a protective effect against oxidative and inflammatory bladder damage induced through the I/R procedure in rats, and evaluate by comparing these compounds. Male rats were divided into five groups: bladder sham-operation applied group (SG); bladder only I/R applied group (IRG); anakinra+bladder I/R applied group (AIR); tocilizumab+bladder I/R applied group (TIR); and ATC+bladder I/R applied group (ATIR). An atraumatic clamp was placed on the abdominal aorta of animals in all groups (except SG), and one hour of ischemia followed by two hours of reperfusion was performed. Our biochemical find-ings showed that anakinra and tocilizumab significantly inhibited the increase of oxidant malondialdehyde (MDA) and the decrease of antioxidants such as total glu-tathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) in bladder tissue by I/R, both at the same levels. Furthermore, anakinra and tocilizumab significantly suppressed the I/R-associated increase of TNF-α, IL-1β, and IL-6 in bladder tissue. ATC was the one that best prevented the I/R-related increase in MDA, TNF-α, IL-1β, and IL-6 and the decrease in tGSH, SOD, and CAT in the bladder tissue. ATC was more beneficial than anakinra or tocilizumab alone in treating bladder I/R damage. © 2023, Instituto de Investigaciones Clinicas. All rights reserved.
dc.identifier.doi10.54817/ic.v64n3a9
dc.identifier.eissn2477-9393
dc.identifier.endpage378
dc.identifier.issn0535-5133
dc.identifier.issue3
dc.identifier.scopus2-s2.0-85174674310
dc.identifier.startpage368
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/12399
dc.identifier.volume64
dc.identifier.wosWOS:001074221100010
dc.language.isoen
dc.publisherInstituto de Investigaciones Clinicas
dc.relation.ispartofInvestigacion Clinica (Venezuela)
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectanakinra
dc.subjectanakinra and tocilizumab combination
dc.subjectbladder
dc.subjectischemia-reperfu-sion damage
dc.subjectrats
dc.subjecttocilizumab
dc.subjectantioxidant
dc.subjectcatalase
dc.subjectglutathione
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectketamine
dc.subjectmalonaldehyde
dc.subjectsuperoxide dismutase
dc.subjecttumor necrosis factor
dc.subjectabdominal aorta
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbladder injury
dc.subjectbladder tissue
dc.subjectcontrolled study
dc.subjectenzyme linked immunosorbent assay
dc.subjectmale
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectprotein analysis
dc.subjectprotein determination
dc.subjectrat
dc.titleEffect of anakinra, tocilizumab, and the combination thereof on bladder ischemia-reperfusion damage in albino Wistar-type rats; [Efecto de la anakinra, el tocilizumab y la combinación de ambos sobre el daño por isquemia-reperfusión vesical en ratas albinas tipo Wistar]
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus2
rdl.citation.wos4
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)