<?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>2026-10-18T23:16:29Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12404" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12404</identifier><datestamp>2026-10-18T21:14:18Z</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>Renoprotective Effect of Taxifolin in Paracetamol-Induced Nephrotoxicity: Emerging Evidence from an Animal Model</dc:title><dc:creator>Topal, Ismail</dc:creator><dc:creator>Özdamar, Mustafa Yaşar</dc:creator><dc:creator>Catakli, Tulin</dc:creator><dc:creator>Malkoc, İsmail</dc:creator><dc:creator>Hacimuftuoglu, Ahmet</dc:creator><dc:creator>Mamoulakis, Charalampos</dc:creator><dc:creator>Tsatsakis, Aristidis</dc:creator><dc:creator>Tsarouhas, Konstantinos</dc:creator><dc:creator>Tsitsimpikou, Christina</dc:creator><dc:creator>Taghizadehghalehjoughi, Ali</dc:creator><dc:subject>acute kidney injury</dc:subject><dc:subject>kidney</dc:subject><dc:subject>nephropathy</dc:subject><dc:subject>paracetamol</dc:subject><dc:subject>renal injury</dc:subject><dc:subject>taxifolin</dc:subject><dc:subject>toxicity</dc:subject><dc:subject>creatinine</dc:subject><dc:subject>glutathione</dc:subject><dc:subject>glutathione peroxidase</dc:subject><dc:subject>glutathione reductase</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:subject>antioxidant activity</dc:subject><dc:subject>Article</dc:subject><dc:subject>blood vessel</dc:subject><dc:subject>cell vacuole</dc:subject><dc:subject>controlled study</dc:subject><dc:subject>creatinine blood level</dc:subject><dc:subject>drug effect</dc:subject><dc:subject>histopathology</dc:subject><dc:subject>kidney tubule epithelium</dc:subject><dc:subject>male</dc:subject><dc:subject>nephrotoxicity</dc:subject><dc:subject>nonhuman</dc:subject><dc:subject>rat</dc:subject><dc:subject>renal protection</dc:subject><dc:subject>urea nitrogen blood level</dc:subject><dc:description>Background: Taxifolin (TXF) is a flavonoid found abundantly in citrus/onion. Encouraging results on its renoprotective effect have been reported in a limited number of drug-induced nephrotoxicity animal models. The present study aimed to evaluate for the first time the potential renoprotective effects of TXF in a paracetamol (PAR)-induced nephrotoxicity rat model. Methods: Rats were divided into three equal groups (n = 6 animals per group). Group 1 (PAR group, PARG) received PAR diluted in normal saline by gavage (1000 mg/kg). Group 2 (TXF group, TXFG) received TXF diluted in normal saline by gavage (50 mg/kg) one hour after PAR administration. Group 3 (control group, CG) received normal saline. Twenty-four hours after PAR administration, all animals were sacrificed using high-dose anesthesia. Blood samples were collected and kidneys were removed. Results: The serum blood urea nitrogen, creatinine levels and serum malondialdehyde levels were significantly increased in the PARG. The serum glutathione peroxidase, glutathione reductase and total glutathione levels were significantly higher in the TXFG. At the same time, the kidneys of the PARG animals demonstrated tubular epithelium swelling, distension and severe vacuolar degeneration. The kidneys of the TXFG animals showed mildly dilated/congested blood vessels. Conclusions: The TXF renoprotective effects are promising in preventing PAR-induced nephrotoxicity, mainly through antioxidant activity, and warrant further testing in future studies. © 2023 by the authors.</dc:description><dc:publisher>MDPI</dc:publisher><dc:date>2023</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/12404</dc:identifier><dc:identifier>https://doi.org/10.3390/jcm12030876</dc:identifier><dc:identifier>2077-0383</dc:identifier><dc:language>en</dc:language><dc:relation>Journal of Clinical Medicine</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/12404</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>