<?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>2026-10-18T23:54:09Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/16609" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/16609</identifier><datestamp>2026-10-18T20:36:29Z</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 Thiamine Pyrophosphate on Amiodarone-Induced Oxidative Kidney Damage in Rats</dc:title><dc:creator>Dagel, Tuncay</dc:creator><dc:creator>Mammadov, Renad</dc:creator><dc:creator>Bulut, Seval</dc:creator><dc:creator>Yeter, Bahtinur</dc:creator><dc:creator>Tastan, Tugba Bal</dc:creator><dc:creator>Ekici, Ozgur</dc:creator><dc:creator>Coban, Taha Abdulkadir</dc:creator><dc:creator>Suleyman, Halis</dc:creator><dc:subject>Amiodarone</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>free oxygen radicals</dc:subject><dc:subject>kidney</dc:subject><dc:subject>oxidative damage</dc:subject><dc:subject>thiamine pyrophosphate</dc:subject><dc:subject>rat</dc:subject><dc:subject>ISCHEMIA-REPERFUSION</dc:subject><dc:subject>STRESS</dc:subject><dc:subject>NEPHROTOXICITY</dc:subject><dc:subject>EXTRACT</dc:subject><dc:subject>Pharmacology &amp; Pharmacy</dc:subject><dc:description>Background and Objective: Amiodarone-induced kidney damage is associated with an increase in oxidant and proinflammatory cytokines. This study was planned to investigate the effect of thiamine pyrophosphate (TPP) on amiodarone-induced oxidative and inflammatory kidney damage in rats on both a biochemical and histopathological basis. Materials and Methods: Albino Wistar-type male rats (6 rats per group) were divided into healthy (HG), amiodarone (ADG) and amiodarone+TPP (TAG) groups. The TPP (20 mg kg(-1)) and amiodarone (50 mg kg(-1)) treatment continued for 14 days. Analyzes of oxidant, antioxidant and proinflammatory cytokines in excised kidney tissues and creatinine and blood urea nitrogen in serum were performed. Results: The amiodarone treated rats showed an increase in malondialdehyde, tumor necrosis factor, interleukin 1 beta, interleukin 6 levels, serum creatinine and blood urea nitrogen in the kidney tissue while a decrease was observed in total glutathione as compared to healthy animals (p&lt;0.001). In addition, histopathological damage occurred in the kidney tissues of the ADG group. It was determined that TPP prevented biochemical changes and histopathological damage significantly (p&lt;0.001). Conclusion: By acting as an antioxidant and anti-inflammatory, TPP might protect kidney tissue from amiodarone-induced damage.</dc:description><dc:publisher>ASIAN NETWORK SCIENTIFIC INFORMATION-ANSINET</dc:publisher><dc:date>2023</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/16609</dc:identifier><dc:identifier>https://doi.org/10.3923/ijp.2023.521.530</dc:identifier><dc:identifier>1811-7775</dc:identifier><dc:language>en</dc:language><dc:relation>INTERNATIONAL JOURNAL OF PHARMACOLOGY</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/16609</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>