Effect of tocilizumab on ischemia-reperfusion-induced oxido-inflammatory renal damage and dysfunction in rats

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Ischemia-reperfusion-induced (I/R) renal damage is a pathogenic process that starts with ischemia, then progresses through oxidative stress and inflammation. Tocilizumab (TCZ), a recombinant human monoclonal antibody produced against the IL-6 receptor, will be tested against renal I/R injury. TCZ is known to lower the levels of proinflammatory cytokines and oxidant mediators while raising the amounts of antioxidant molecules. Our purpose is to evaluate the biochemical and histological effects of TCZ against I/R-induced oxido-inflammatory kidney damage and dysfunction in rats. Animals were divided into 3 groups as renal I/R (RIR), I/R+ TCZ (IRT), and healthy group (HG). TCZ was administered at a dose of 8 mg/kg to the IRT group (n=6) of the animals, and distilled water as a solvent was administered intraperitoneally (ip) to the RIR (n=6) and HG (n=6) groups. Then, two hours of ischemia and six hours of reperfusion were applied to the left kidneys of IRT and RIR animals. TCZ significantly inhibited the increase in the levels of malondialdehyde (MDA), nuclear kappa B (NF-κB), tumour necrosis factor alpha (TNF-α), interleukin 1-β (IL-1β), IL-6, creatinine (Cr) and blood urea nitrogen (BUN) and decrease in total glutathione (tGSH) with I/R in renal tissue. TCZ also attenuated severe histopathological damage due to I/R in renal tissue. TCZ protected renal tissue from I/R-induced oxidative and inflammatory damage. These results indicate that TCZ may be useful in the treatment of renal I/R injury. © 2022 Japanese Association for Laboratory Animal Science.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/13005Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1538/expanim.22-0034Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorErdem, Kezban Tuna Ozkaloglu
dc.contributor.authorBedir, Zehra
dc.contributor.authorKuyrukluyildiz, Ufuk
dc.contributor.authorTas, Hakan Gokalp
dc.contributor.authorSuleyman, Zeynep
dc.contributor.authorBulut, Seval
dc.contributor.authorMendil, Ali Sefa
dc.contributor.authorSarigul, Cengiz
dc.contributor.authorUnver, Edhem
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:27:51.335797478Z
dc.date.available2026-10-18T20:27:51.335797478Z
dc.date.issued2022
dc.description.abstractIschemia-reperfusion-induced (I/R) renal damage is a pathogenic process that starts with ischemia, then progresses through oxidative stress and inflammation. Tocilizumab (TCZ), a recombinant human monoclonal antibody produced against the IL-6 receptor, will be tested against renal I/R injury. TCZ is known to lower the levels of proinflammatory cytokines and oxidant mediators while raising the amounts of antioxidant molecules. Our purpose is to evaluate the biochemical and histological effects of TCZ against I/R-induced oxido-inflammatory kidney damage and dysfunction in rats. Animals were divided into 3 groups as renal I/R (RIR), I/R+ TCZ (IRT), and healthy group (HG). TCZ was administered at a dose of 8 mg/kg to the IRT group (n=6) of the animals, and distilled water as a solvent was administered intraperitoneally (ip) to the RIR (n=6) and HG (n=6) groups. Then, two hours of ischemia and six hours of reperfusion were applied to the left kidneys of IRT and RIR animals. TCZ significantly inhibited the increase in the levels of malondialdehyde (MDA), nuclear kappa B (NF-κB), tumour necrosis factor alpha (TNF-α), interleukin 1-β (IL-1β), IL-6, creatinine (Cr) and blood urea nitrogen (BUN) and decrease in total glutathione (tGSH) with I/R in renal tissue. TCZ also attenuated severe histopathological damage due to I/R in renal tissue. TCZ protected renal tissue from I/R-induced oxidative and inflammatory damage. These results indicate that TCZ may be useful in the treatment of renal I/R injury. © 2022 Japanese Association for Laboratory Animal Science.
dc.identifier.doi10.1538/expanim.22-0034
dc.identifier.eissn1881-7122
dc.identifier.endpage499
dc.identifier.issn1341-1357
dc.identifier.issue4
dc.identifier.pmcidPMC9671765
dc.identifier.pmid35781445
dc.identifier.scopus2-s2.0-85141732642
dc.identifier.startpage491
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13005
dc.identifier.volume71
dc.identifier.wosWOS:001127021500013
dc.language.isoen
dc.publisherInternational Press Editing Centre Incorporation
dc.relation.ispartofExperimental Animals
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectischemia/reperfusion
dc.subjectkidney
dc.subjectoxidative stress
dc.subjecttocilizumab
dc.subjectAcute Kidney Injury
dc.subjectAnimals
dc.subjectHumans
dc.subjectRats
dc.subjectReperfusion
dc.subjectReperfusion Injury
dc.subjectanesthetic agent
dc.subjectinterleukin 10
dc.subjectinterleukin 6
dc.subjectketamine
dc.subjectmalonaldehyde
dc.subjectmonoclonal antibody
dc.subjectreactive oxygen metabolite
dc.subjectxylazine
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbiochemical analysis
dc.subjectenzyme linked immunosorbent assay
dc.subjecthistopathology
dc.subjectkidney function
dc.subjectkidney injury
dc.subjectkidney ischemia
dc.subjectlipid peroxidation
dc.subjectmale
dc.subjectnonhuman
dc.titleEffect of tocilizumab on ischemia-reperfusion-induced oxido-inflammatory renal damage and dysfunction in rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus12
rdl.citation.wos14
rdl.departmentDepartment of Anesthesiology and Reanimation, Faculty of Medicine, Erzincan Binali Yildirim University, Associate Professor, Başbağlar Mahallesi 1429. Street No:2/1 24100 Erzincan, Turkey. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University, Başbağlar Mahallesi 1429. Street No:2/1 24100 Erzincan, Turkey. | Department of Biochemistry, Faculty of Medicine, Erzincan Binali Yildirim University, Başbağlar Mahallesi 1429. Street No:2/1 24100 Erzincan, Turkey. | Department of Chest Diseases, Faculty of Medicine, Erzincan Binali Yildirim University, Başbağlar Mahallesi 1429. Street No:2/1 24100 Erzincan, Turkey.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)