Effect of taxifolin on development of retinopathy in alloxan-induced diabetic rats

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Purpose: Diabetic retinopathy (DR) is one of the leading causes of blindness. In DR patients, antioxidant defence is disrupted, and production of reactive oxygen species and pro-inflammatory cytokines such as interleukin 1β (IL-1β) and tumour necrosis factor alpha (TNF-α) increases. Taxifolin has been reported to suppress reactive oxygen species, IL-1β and TNF-α production. The aim of this study is to biochemically and histopathologically examine the protective effect of taxifolin against DR damage induced by alloxan. Materials and methods: Alloxan received rats with a blood glucose level of ≥250 mg/dL were divided into taxifolin-treated (TAX) (n = 6), diabetic control (DC) (n = 6) groups. There were rats received only saline in non-diabetic control (NC) group (n = 6). Taxifolin (50 mg/kg) was orally administered to the TAX group rats. DC and NC rats received the same volume of saline as a solvent. This procedure was repeated once a day for 3 months. At the end of this period, animals were killed by high dose thiopental sodium anaesthesia. Histopathological examinations were then performed on excised rat eyes. Malondialdehyde (MDA), total glutathione (tGSH), IL-1β and TNF-α levels were measured in obtained blood samples. Results: MDA, IL-1β and TNF-α levels were significantly increased in blood samples of DC group rats with hyperglycemia induced by alloxan compared with NC group (p < 0.0001), and decreased in the TAX group compared with the DC group (p < 0.0001). The levels of tGSH were significantly decreased in blood samples of DC group rats compared with NC group (p < 0.0001), and increased in the TAX group compared with the DC group (p < 0.0001). Histopathologically, retinal ganglion cells of the TAX group had a slightly dilated and congested blood vessel, and severe damage was inflicted to the retinal ganglion cell layer of the DC group. Conclusions: Experimental results suggest that taxifolin may be beneficial in the treatment of DR. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.

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AlanDeğerDil
dc.contributor.authorAhiskali, Ibrahim
dc.contributor.authorPinar, Can Lokman
dc.contributor.authorKiki, Murat
dc.contributor.authorMammadov, Renad
dc.contributor.authorOzbek Bilgin, Asli
dc.contributor.authorHacimuftuoglu, Ahmet
dc.contributor.authorCankaya, Murat
dc.contributor.authorKeskin Cimen, Ferda
dc.contributor.authorAltuner, Durdu
dc.date.accessioned2026-10-18T20:28:35.682654682Z
dc.date.available2026-10-18T20:28:35.682654682Z
dc.date.issued2019
dc.description.abstractPurpose: Diabetic retinopathy (DR) is one of the leading causes of blindness. In DR patients, antioxidant defence is disrupted, and production of reactive oxygen species and pro-inflammatory cytokines such as interleukin 1β (IL-1β) and tumour necrosis factor alpha (TNF-α) increases. Taxifolin has been reported to suppress reactive oxygen species, IL-1β and TNF-α production. The aim of this study is to biochemically and histopathologically examine the protective effect of taxifolin against DR damage induced by alloxan. Materials and methods: Alloxan received rats with a blood glucose level of ≥250 mg/dL were divided into taxifolin-treated (TAX) (n = 6), diabetic control (DC) (n = 6) groups. There were rats received only saline in non-diabetic control (NC) group (n = 6). Taxifolin (50 mg/kg) was orally administered to the TAX group rats. DC and NC rats received the same volume of saline as a solvent. This procedure was repeated once a day for 3 months. At the end of this period, animals were killed by high dose thiopental sodium anaesthesia. Histopathological examinations were then performed on excised rat eyes. Malondialdehyde (MDA), total glutathione (tGSH), IL-1β and TNF-α levels were measured in obtained blood samples. Results: MDA, IL-1β and TNF-α levels were significantly increased in blood samples of DC group rats with hyperglycemia induced by alloxan compared with NC group (p < 0.0001), and decreased in the TAX group compared with the DC group (p < 0.0001). The levels of tGSH were significantly decreased in blood samples of DC group rats compared with NC group (p < 0.0001), and increased in the TAX group compared with the DC group (p < 0.0001). Histopathologically, retinal ganglion cells of the TAX group had a slightly dilated and congested blood vessel, and severe damage was inflicted to the retinal ganglion cell layer of the DC group. Conclusions: Experimental results suggest that taxifolin may be beneficial in the treatment of DR. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.
dc.identifier.doi10.1080/15569527.2019.1588289
dc.identifier.eissn1556-9535
dc.identifier.endpage232
dc.identifier.issn1556-9527
dc.identifier.issue3
dc.identifier.pmid30897968
dc.identifier.scopus2-s2.0-85063205553
dc.identifier.startpage227
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13777
dc.identifier.volume38
dc.identifier.wosWOS:000463405300001
dc.language.isoen
dc.publisherTaylor and Francis Ltd
dc.relation.ispartofCutaneous and Ocular Toxicology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAlloxan
dc.subjectdiabetic retinopathy
dc.subjectrat
dc.subjectretina toxicity
dc.subjecttaxifolin
dc.subjectAnimals
dc.subjectAnti-Inflammatory Agents, Non-Steroidal
dc.subjectDiabetes Mellitus, Experimental
dc.subjectGlutathione
dc.subjectInterleukin-1beta
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectQuercetin
dc.subjectRats, Wistar
dc.subjectRetinal Ganglion Cells
dc.subjectTumor Necrosis Factor-alpha
dc.subjectglucose
dc.subjectinterleukin 1beta
dc.subjectmalonaldehyde
dc.subjectreactive oxygen metabolite
dc.subjecttumor necrosis factor
dc.subjectIL1B protein, human
dc.subjectnonsteroid antiinflammatory agent
dc.subjectalloxan-induced diabetes mellitus
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbiochemical analysis
dc.subjectblindness
dc.titleEffect of taxifolin on development of retinopathy in alloxan-induced diabetic rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus36
rdl.citation.wos34
rdl.departmentb Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University , Erzincan , Turkey. | d Department of Biology, Faculty of Science and Art, Erzincan Binali Yildirim University , Erzincan , Turkey. | e Department of Pathology, Faculty of Medicine, Erzincan Binali Yildirim University , Erzincan , Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)