<?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>2026-10-19T00:02:36Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11655" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/11655</identifier><datestamp>2026-10-18T21:13:17Z</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>AuNPs with Cynara scolymus leaf extracts rescue arsenic-induced neurobehavioral deficits and hippocampal tissue toxicity in Balb/c mice through D1R and D2R activation</dc:title><dc:creator>Cicek, Betul</dc:creator><dc:creator>Hacimuftuoglu, Ahmet</dc:creator><dc:creator>Yeni, Yesim</dc:creator><dc:creator>Kuzucu, Mehmet</dc:creator><dc:creator>Genc, Sidika</dc:creator><dc:creator>Cetin, Ahmet</dc:creator><dc:creator>Yavuz, Emre</dc:creator><dc:creator>Danısman, Betul</dc:creator><dc:creator>Levent, Akin</dc:creator><dc:creator>Ozdokur, Kemal Volkan</dc:creator><dc:creator>Kantarcı, Mecit</dc:creator><dc:creator>Docea, Anca Oana</dc:creator><dc:creator>Siokas, Vasileios</dc:creator><dc:creator>Tsarouhas, Konstantinos</dc:creator><dc:creator>Coleman, Michael D.</dc:creator><dc:creator>Tsatsakis, Aristidis</dc:creator><dc:creator>Taghizadehghalehjoughi, Ali</dc:creator><dc:subject>Arsenic</dc:subject><dc:subject>AuNPs</dc:subject><dc:subject>Cynara scolymus</dc:subject><dc:subject>D1R</dc:subject><dc:subject>D2R</dc:subject><dc:subject>Neurotoxicity</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Gold</dc:subject><dc:subject>Hippocampus</dc:subject><dc:subject>Metal Nanoparticles</dc:subject><dc:subject>Mice</dc:subject><dc:subject>Mice, Inbred BALB C</dc:subject><dc:subject>Plant Extracts</dc:subject><dc:subject>arsenite sodium</dc:subject><dc:subject>caspase 3</dc:subject><dc:subject>Cynara scolymus extract</dc:subject><dc:subject>dopamine 1 receptor</dc:subject><dc:subject>dopamine 2 receptor</dc:subject><dc:subject>gold nanoparticle</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>messenger RNA</dc:subject><dc:subject>protein Bax</dc:subject><dc:subject>protein bcl 2</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>artichoke leaf</dc:subject><dc:subject>metal nanoparticle</dc:subject><dc:subject>plant extract</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:description>The present study was designed to evaluate whether AuNPs (gold nanoparticles) synthesized with the Cynara scolymus (CS) leaf exert protective and/or alleviative effects on arsenic (As)-induced hippocampal neurotoxicity in mice. Neurotoxicity in mice was developed by orally treating 10 mg/kg/day sodium arsenite (NaAsO2) for 21 days. 10 µg/g AuNPs, 1.6 g/kg CS, and 10 µg/g CS-AuNPs were administered orally simultaneously with 10 mg/kg As. CS and CS-AuNPs treatments showed down-regulation of TNF-α and IL-1β levels. CS and CS-AuNPs also ameliorated apoptosis and reduced the alterations in the expression levels of D1 and D2 dopamine receptors induced by As. Simultaneous treatment with CS and CS-AuNPs improved As-induced learning, memory deficits, and motor coordination in mice assessed by water maze and locomotor tests, respectively. The results of this study provide evidence that CS-AuNPs demonstrated neuroprotective roles with antioxidant, anti-inflammatory, and anti-apoptotic effects, as well as improving D1 and D2 signaling, and eventually reversed neurobehavioral impairments. © 2024 Elsevier B.V.</dc:description><dc:publisher>Elsevier B.V.</dc:publisher><dc:date>2024</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/11655</dc:identifier><dc:identifier>https://doi.org/10.1016/j.etap.2024.104417</dc:identifier><dc:identifier>1382-6689</dc:identifier><dc:language>en</dc:language><dc:relation>Environmental Toxicology and 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/11655</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>