<?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>2026-10-18T23:15:56Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10141" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10141</identifier><datestamp>2026-10-18T21:13:12Z</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>Effects of apigenin, hesperidin and their combinations on different physiopathological pathways in 5-fluorouracil-induced pulmonary damage</dc:title><dc:creator>Uslu, Hamit</dc:creator><dc:creator>Atila Uslu, Gözde</dc:creator><dc:creator>Çoban, Taha Abdulkadir</dc:creator><dc:creator>Özkaraca, Mustafa</dc:creator><dc:creator>Kurt, Nezahat</dc:creator><dc:creator>Mendil, Ali Sefa</dc:creator><dc:subject>5-fluorouracil</dc:subject><dc:subject>apigenin</dc:subject><dc:subject>apoptosis</dc:subject><dc:subject>hesperidin</dc:subject><dc:subject>lung damage</dc:subject><dc:subject>MAPK/NFκB</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antimetabolites, Antineoplastic</dc:subject><dc:subject>Autophagy</dc:subject><dc:subject>Caspase 3</dc:subject><dc:subject>Fluorouracil</dc:subject><dc:subject>Lung</dc:subject><dc:subject>Male</dc:subject><dc:subject>NF-kappa B</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Rats</dc:subject><dc:subject>antineoplastic antimetabolite</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>animal</dc:subject><dc:subject>drug effect</dc:subject><dc:subject>metabolism</dc:subject><dc:subject>pathology</dc:subject><dc:subject>rat</dc:subject><dc:description>Background: Chemotherapeutics target cancerous cells, but they also have unavoidable toxicities in healthy tissues. Aim: In this study, the effects of the commonly used chemotherapeutic 5-fluorouracil (5FU) on lung tissue were investigated, along with the possible protective benefits of apigenin (API), hesperidin (HES), and their combination. Methodology: The study consisted of control, 5FU, API + 5FU, HES + 5FU, and API+HES + 5FU groups. API 50 mg/kg and HES 200 mg/kg were administered for 7 days. On the 8th day, 5FU was administered a dose of 100 mg/kg. Results: Analyses showed that API and HES were effective in preventing oxidative stress induced by 5FU in lung tissue, attenuating inflammation and apoptosis by suppressing MAPK/NFκB and Caspase-3/Bax/Bcl-2 pathways, suppressing autophagy by decreasing LC3B expression, and regulating Sigmar1 expression. Conclusion: These results suggest that the two flavonoids, when administered separately or in combination, may be useful in reducing side effects that often occur during the use of chemotherapeutics. © 2025 Informa UK Limited, trading as Taylor &amp; Francis Group.</dc:description><dc:publisher>Taylor and Francis Ltd.</dc:publisher><dc:date>2026</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/10141</dc:identifier><dc:identifier>https://doi.org/10.1080/13813455.2025.2531443</dc:identifier><dc:identifier>1381-3455</dc:identifier><dc:language>en</dc:language><dc:relation>Archives of Physiology and Biochemistry</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/10141</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>