<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-19T04:52:29Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13777" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13777</identifier><datestamp>2026-10-18T21:13:30Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Effect of taxifolin on development of retinopathy in alloxan-induced diabetic rats</dc:title><dc:creator>Ahiskali, Ibrahim</dc:creator><dc:creator>Pinar, Can Lokman</dc:creator><dc:creator>Kiki, Murat</dc:creator><dc:creator>Mammadov, Renad</dc:creator><dc:creator>Ozbek Bilgin, Asli</dc:creator><dc:creator>Hacimuftuoglu, Ahmet</dc:creator><dc:creator>Cankaya, Murat</dc:creator><dc:creator>Keskin Cimen, Ferda</dc:creator><dc:creator>Altuner, Durdu</dc:creator><dc:subject>Alloxan</dc:subject><dc:subject>diabetic retinopathy</dc:subject><dc:subject>rat</dc:subject><dc:subject>retina toxicity</dc:subject><dc:subject>taxifolin</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Anti-Inflammatory Agents, Non-Steroidal</dc:subject><dc:subject>Diabetes Mellitus, Experimental</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Interleukin-1beta</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>Quercetin</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Retinal Ganglion Cells</dc:subject><dc:subject>Tumor Necrosis Factor-alpha</dc:subject><dc:subject>glucose</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>reactive oxygen metabolite</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>IL1B protein, human</dc:subject><dc:subject>nonsteroid antiinflammatory agent</dc:subject><dc:subject>alloxan-induced diabetes mellitus</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>Article</dc:subject><dc:subject>biochemical analysis</dc:subject><dc:subject>blindness</dc:subject><dc:description>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 &lt; 0.0001), and decreased in the TAX group compared with the DC group (p &lt; 0.0001). The levels of tGSH were significantly decreased in blood samples of DC group rats compared with NC group (p &lt; 0.0001), and increased in the TAX group compared with the DC group (p &lt; 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 &amp; Francis Group.</dc:description><dc:publisher>Taylor and Francis Ltd</dc:publisher><dc:date>2019</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/13777</dc:identifier><dc:identifier>https://doi.org/10.1080/15569527.2019.1588289</dc:identifier><dc:identifier>1556-9527</dc:identifier><dc:language>en</dc:language><dc:relation>Cutaneous and Ocular Toxicology</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/13777</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>