<?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>2026-10-19T01:40:09Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11425" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11425</identifier><datestamp>2026-10-18T21:13:16Z</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>Hepatoprotective effects of resveratrol on α-amanitin-induced liver toxicity in rats</dc:title><dc:creator>Gezer, Arzu</dc:creator><dc:creator>Ustundag, Hilal</dc:creator><dc:creator>Mendil, Ali Sefa</dc:creator><dc:creator>Bedir, Gursel</dc:creator><dc:creator>Duysak, Lale</dc:creator><dc:subject>Hepatotoxicity</dc:subject><dc:subject>Inflammation</dc:subject><dc:subject>Oxidative stress</dc:subject><dc:subject>Resveratrol</dc:subject><dc:subject>α-Amanitin</dc:subject><dc:subject>Alpha-Amanitin</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Apoptosis</dc:subject><dc:subject>Chemical and Drug Induced Liver Injury</dc:subject><dc:subject>Liver</dc:subject><dc:subject>Male</dc:subject><dc:subject>Protective Agents</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Sprague-Dawley</dc:subject><dc:subject>Stilbenes</dc:subject><dc:subject>alanine aminotransferase</dc:subject><dc:subject>alpha amanitin</dc:subject><dc:subject>aspartate aminotransferase</dc:subject><dc:subject>catalase</dc:subject><dc:subject>glutathione peroxidase</dc:subject><dc:subject>glutathione reductase</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>myeloperoxidase</dc:subject><dc:subject>nitric oxide synthase</dc:subject><dc:subject>reduced nicotinamide adenine dinucleotide phosphate</dc:subject><dc:subject>sevoflurane</dc:subject><dc:subject>thiopental</dc:subject><dc:subject>antioxidant</dc:subject><dc:description>Objective: The hepatoprotective effects of resveratrol against α-Amanitin (α-AMA)-induced liver toxicity were investigated in an experimental rat model, focusing on oxidative stress, inflammation, apoptosis, and liver function. Methods: Thirty-two male Sprague-Dawley rats were divided into four groups (n = 8 per group): Control, resveratrol, α-AMA, and resveratrol+α-AMA. The resveratrol group received 20 mg/kg resveratrol orally for 7 days. The α-AMA group received 3 mg/kg α-AMA intraperitoneally on the 8th day. The resveratrol+α-AMA group received 20 mg/kg resveratrol orally (7 days) followed by 3 mg/kg α-AMA intraperitoneally on the 8th day. Liver tissues and blood samples were collected 48 h after α-amanitin administration for histopathological, immunohistochemical (NFkB, LC3B), and biochemical analyses (GSH, MDA, CAT, GPx, MPO, NOS, AST, ALT). Results: α-AMA significantly increased AST and ALT levels, oxidative stress marker (MDA), and inflammatory marker (MPO), while reducing antioxidant levels (GSH, CAT, GPx) and NOS concentration (P &lt; 0.001 for all parameters). Histopathological analysis showed severe liver damage with increased NFkB and LC3B expression. resveratrol treatment significantly reduced AST and ALT levels (P &lt; 0.01 for both parameters), decreased MDA and MPO levels, and increased NOS concentration, GSH, CAT, and GPx levels (P &lt; 0.05 for all parameters). Reduced NFkB and LC3B expression in the resveratrol+α-AMA group and showed histopathological improvements. Conclusion: Resveratrol demonstrated substantial hepatoprotective effects against α-AMA induced liver toxicity by reducing oxidative stress, inflammation, and apoptosis, and improving liver function. These findings suggest that resveratrol could be a potential therapeutic agent for treating liver damage caused by potent hepatotoxins like α-AMA. © 2024 Elsevier Ltd</dc:description><dc:publisher>Elsevier Ltd</dc:publisher><dc:date>2024</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/11425</dc:identifier><dc:identifier>https://doi.org/10.1016/j.toxicon.2024.107855</dc:identifier><dc:identifier>0041-0101</dc:identifier><dc:language>en</dc:language><dc:relation>Toxicon</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/11425</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>