<?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>2026-10-19T01:43:08Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/16471" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/16471</identifier><datestamp>2026-10-18T20:34:10Z</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>Research Article Potent Protective Effect of Lacidipine, Carvacrol and Lacidipine-Carvacrol Combination Against 5-Fluorouracil-Induced Cardiotoxicity in Rats</dc:title><dc:creator>Akbas, Nergis</dc:creator><dc:creator>Suleyman, Halis</dc:creator><dc:subject>Cardiotoxicity</dc:subject><dc:subject>carvacrol</dc:subject><dc:subject>fluorouracil</dc:subject><dc:subject>inflammation</dc:subject><dc:subject>lacidipine</dc:subject><dc:subject>oxidative stress</dc:subject><dc:subject>ANTIOXIDANT</dc:subject><dc:subject>INTERLEUKIN-6</dc:subject><dc:subject>ACTIVATION</dc:subject><dc:subject>CHANNEL</dc:subject><dc:subject>CELLS</dc:subject><dc:subject>Pharmacology &amp; Pharmacy</dc:subject><dc:description>Background and Objective: 5-Fluorouracil (5-FU) is the second most common cardiotoxic chemotherapeutic drug. Inflammation and oxidative stress are implicated in the pathogenesis of 5- FU-induced cardiotoxicity. This study evaluated the effectiveness of lacidipine and carvacrol, which have anti-inflammatory and antioxidant properties, against 5-FU-induced cardiotoxicity. Materials and Methods: Rats were divided into a control group (HC) and groups receiving 5-FU (FU), 5-FU+lacidipine (LFU), 5-FU+carvacrol (CFU), or 5-FU+lacidipine+carvacrol (LCFU). Malondialdehyde (MDA), Glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and Interleukin-6 (IL-6) from heart tissue and Creatine Kinase MB (CK-MB) and troponin I (TP-I) from plasma were evaluated. Results: The SOD and CAT activities and GSH levels were significantly lower in the FU group than HC, LFU, CFU and LCFU groups (p&lt;0.001). The MDA, IL-6, TP-I and CK-MB levels were significantly higher in the FU group than HC, LFU, CFU and LCFU groups (p&lt;0.001). Differences between HC and LCFU groups were detected only in terms of GSH (p = 0.09). Conclusion: The lacidipine and carvacrol are effective against 5-FU-induced cardiotoxicity, but a combination is more effective.</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/16471</dc:identifier><dc:identifier>https://doi.org/10.3923/ijp.2023.321.328</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/16471</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>