<?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>2026-10-19T01:56:51Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10921" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/10921</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>Panax Ginseng Protects Against Doxorubicin-Induced Testicular Injury in Male Rats by Modulating NF-κB/COX-2 and AR Pathways</dc:title><dc:creator>Yeni, Yesim</dc:creator><dc:creator>Cicek, Betul</dc:creator><dc:creator>Hacimuftuoglu, Ahmet</dc:creator><dc:creator>Ozkaraca, Mustafa</dc:creator><dc:creator>Mokhtare, Behzad</dc:creator><dc:subject>Doxorubicin</dc:subject><dc:subject>Male Fertility</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Panax Ginseng</dc:subject><dc:subject>Real-Time PCR</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Cyclooxygenase 2</dc:subject><dc:subject>Male</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>NF-kappa B</dc:subject><dc:subject>Panax</dc:subject><dc:subject>Plant Extracts</dc:subject><dc:subject>Protective Agents</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Sprague-Dawley</dc:subject><dc:subject>Receptors, Androgen</dc:subject><dc:subject>Signal Transduction</dc:subject><dc:subject>Testis</dc:subject><dc:subject>Testosterone</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>catalase</dc:subject><dc:subject>follitropin</dc:subject><dc:subject>ginseng extract</dc:subject><dc:subject>glutathione</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>lactate dehydrogenase</dc:subject><dc:subject>luteinizing hormone</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>superoxide dismutase</dc:subject><dc:subject>thiopental</dc:subject><dc:description>Panax ginseng (PG) is a medicinal plant used for many years to treat many diseases. The current study aimed to investigate the possible prophylactic and therapeutic effects of PG extract on doxorubicin (DOX)-induced testicular toxicity in rats. 32 adult male Sprague–Dawley rats (200–250 g) were used in the experiment. The experimental groups were designed as control (normal saline, intraperitoneal), DOX (18 mg/kg, intraperitoneal), PG (200 mg/kg, gavage), and PG + DOX (200 mg/kg, gavage). After treatment, serum levels of testosterone, interleukin-1β (IL-1β), glutathione (GSH), luteinizing hormone (LH), superoxide dismutase (SOD), lactate dehydrogenase (LDH), catalase (CAT), follicle stimulating hormone (FSH), tumor necrosis factor-α (TNF-α), and malondialdehyde (MDA) were measured. Then, gene expression, histopathological, and immunohistochemical analyses were performed on testicular tissues. Compared to DOX, treatment with PG + DOX showed a significant improvement in serum levels of FSH, testosterone, LH, TNF-α, IL-1β, MDA, SOD, LDH, GSH, and CAT. It was also observed that PG + DOX decreased nuclear factor-κB and cyclooxygenase-2 expression levels, increased androgen receptor expression, restored testicular histopathological structure, and significantly improved spermatogenesis. The results of the present study showed that PG may have an ameliorative effect against DOX-induced male reproductive toxicity, as DOX causes male reproductive toxicity. It can be concluded that PG is one of the effects that protect against DOX-induced testicular toxicity in rats by reducing lipid peroxidation and activating the antioxidant system. In light of this information, PG may be a useful agent to prevent the testicular toxicity observed in men receiving DOX treatment. © The Author(s) 2025.</dc:description><dc:publisher>Springer</dc:publisher><dc:date>2025</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/10921</dc:identifier><dc:identifier>https://doi.org/10.1007/s12035-025-05116-9</dc:identifier><dc:identifier>0893-7648</dc:identifier><dc:language>en</dc:language><dc:relation>Molecular Neurobiology</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/10921</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>