Comparative Protective Effects of Anakinra and Tocilizumab in Experimental Ocular Ischemic Syndrome

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Özet

Ocular ischemic syndrome (OIS) is a vision-threatening disorder characterized by retinal ischemia, oxidative stress, and inflammation. In this study, the protective effects of anakinra, an interleukin-1 receptor antagonist, were investigated and compared with those of tocilizumab, an interleukin-6 receptor antagonist. Twenty-four male Wistar rats were randomly assigned to four groups (n = 6 per group): sham-operated (SG), carotid artery clamping/unclamping (CUG), anakinra-treated carotid artery clamping/unclamping (ACUG), and tocilizumab-treated carotid artery clamping/unclamping (TCUG). An experimental ocular ischemic injury model induced by transient bilateral common carotid artery occlusion was established by transient bilateral common carotid artery clamping followed by reperfusion. Retinal tissues were analyzed for malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) levels, and histopathological examinations were performed. OIS markedly increased MDA, TNF-α, IL-1β, and IL-6 levels while significantly decreasing tGSH, SOD, and CAT activities. Both anakinra and tocilizumab attenuated oxidative stress and inflammatory responses; however, anakinra produced notably greater improvements in MDA, tGSH, SOD, and CAT levels. Histopathological evaluation demonstrated that both treatments reduced retinal injury, edema, vascular congestion, and inflammatory cell infiltration. Although retinal architecture appeared slightly better preserved in the anakinra-treated group, histopathological scores were comparable between the treatment groups. These findings suggest that anakinra may attenuate oxidative and inflammatory retinal damage in this experimental ocular ischemic injury model and may provide greater biochemical protection than tocilizumab, whereas histopathological protection was comparable between treatments. Nevertheless, further experimental and clinical studies are required to confirm these findings. © 2026 by the authors.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/10249Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.3390/ijms27157029Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorKarimov, Shavkatbek
dc.contributor.authorSezgin, Esra Tuba
dc.contributor.authorMammadov, Renad
dc.contributor.authorSuleyman, Bahadir
dc.contributor.authorYaqudov, Kamandar
dc.contributor.authorYazici, Gulce Naz
dc.contributor.authorCoban, Taha Abdulkadir
dc.contributor.authorSuleyman, Halis
dc.contributor.authorBayrakceken, Kemal
dc.date.accessioned2026-10-18T20:25:29.936076378Z
dc.date.available2026-10-18T20:25:29.936076378Z
dc.date.issued2026
dc.description.abstractOcular ischemic syndrome (OIS) is a vision-threatening disorder characterized by retinal ischemia, oxidative stress, and inflammation. In this study, the protective effects of anakinra, an interleukin-1 receptor antagonist, were investigated and compared with those of tocilizumab, an interleukin-6 receptor antagonist. Twenty-four male Wistar rats were randomly assigned to four groups (n = 6 per group): sham-operated (SG), carotid artery clamping/unclamping (CUG), anakinra-treated carotid artery clamping/unclamping (ACUG), and tocilizumab-treated carotid artery clamping/unclamping (TCUG). An experimental ocular ischemic injury model induced by transient bilateral common carotid artery occlusion was established by transient bilateral common carotid artery clamping followed by reperfusion. Retinal tissues were analyzed for malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) levels, and histopathological examinations were performed. OIS markedly increased MDA, TNF-α, IL-1β, and IL-6 levels while significantly decreasing tGSH, SOD, and CAT activities. Both anakinra and tocilizumab attenuated oxidative stress and inflammatory responses; however, anakinra produced notably greater improvements in MDA, tGSH, SOD, and CAT levels. Histopathological evaluation demonstrated that both treatments reduced retinal injury, edema, vascular congestion, and inflammatory cell infiltration. Although retinal architecture appeared slightly better preserved in the anakinra-treated group, histopathological scores were comparable between the treatment groups. These findings suggest that anakinra may attenuate oxidative and inflammatory retinal damage in this experimental ocular ischemic injury model and may provide greater biochemical protection than tocilizumab, whereas histopathological protection was comparable between treatments. Nevertheless, further experimental and clinical studies are required to confirm these findings. © 2026 by the authors.
dc.identifier.doi10.3390/ijms27157029
dc.identifier.eissn1422-0067
dc.identifier.issn1661-6596
dc.identifier.issue15
dc.identifier.pmcidPMC13467194
dc.identifier.pmid42589680
dc.identifier.scopus2-s2.0-105047150451
dc.identifier.startpage7029
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/10249
dc.identifier.volume27
dc.identifier.wosWOS:001846886500001
dc.language.isoen
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI)
dc.relation.ispartofInternational Journal of Molecular Sciences
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectanakinra
dc.subjectIL-1β
dc.subjectIL-6
dc.subjectinflammation
dc.subjectischemia–reperfusion injury
dc.subjectocular ischemic syndrome
dc.subjectoxidative stress
dc.subjectretinal ischemia
dc.subjecttocilizumab
dc.subjectAnimals
dc.subjectAntibodies, Monoclonal, Humanized
dc.subjectDisease Models, Animal
dc.subjectInterleukin 1 Receptor Antagonist Protein
dc.subjectInterleukin-1beta
dc.subjectInterleukin-6
dc.subjectIschemia
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReperfusion Injury
dc.subjectRetina
dc.subjectSuperoxide Dismutase
dc.subjectTumor Necrosis Factor-alpha
dc.subjectcatalase
dc.subjectglutathione
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectmalonaldehyde
dc.subjecttumor necrosis factor
dc.titleComparative Protective Effects of Anakinra and Tocilizumab in Experimental Ocular Ischemic Syndrome
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus0
rdl.citation.wos0
rdl.departmentDepartment of Ophthalmology, Mengücek Gazi Training and Research Hospital, Erzincan 24100, Turkey. | Anesthesia Program, Vocational School of Health Services, Erzincan Binali Yıldırım University, Erzincan 24100, Turkey. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan 24100, Turkey. | Department of Histology and Embryology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan 24100, Turkey. | Department of Medical Biochemistry, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan 24100, Turkey.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)