{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T07:25:54Z","timestamp":1786951554627,"version":"build-2736575974"},"reference-count":28,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Methotrexate (MTX)\u2010induced nephrotoxicity remains a clinically relevant limitation associated with oxidative stress, inflammation, and apoptosis. Dexpanthenol (DEX), a pantothenic acid derivative, has demonstrated cytoprotective properties; however, its effects on MTX\u2010induced renal injury and related molecular pathways are not fully elucidated. This study investigated the potential renoprotective effects of DEX with a focus on inflammation\u2010 and redox\u2010associated signaling. Thirty\u2010two male Wistar rats were allocated into four groups: Control, MTX, MTX\u2009+\u2009DEX, and DEX. Renal injury was assessed by histopathology, immunohistochemical analysis of caspase\u20103, NF\u2010\u03baB, and TNF\u2010\u03b1, biochemical parameters (urea and creatinine), and RT\u2010qPCR analysis of SIRT1, PGC\u20101\u03b1, NRF2, and HO\u20101 gene expression. MTX administration resulted in marked renal damage characterized by tubular degeneration, hyperemia, and inflammatory infiltration, accompanied by increased caspase\u20103, NF\u2010\u03baB, and TNF\u2010\u03b1 expression (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). MTX also significantly suppressed SIRT1, PGC\u20101\u03b1, NRF2, and HO\u20101 gene expression (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). DEX co\u2010treatment attenuated histopathological injury and significantly reduced pro\u2010inflammatory and apoptotic markers while restoring SIRT1, PGC\u20101\u03b1, and HO\u20101 expression (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.01\u20130.001), with a non\u2010significant upward trend in NRF2 levels. Biochemically, DEX reduced MTX\u2010induced urea and creatinine elevation. DEX confers significant protection against MTX\u2010induced renal injury, likely through modulation of inflammatory and oxidative stress\u2013related regulatory pathways and attenuation of apoptosis. These findings support the potential of DEX as a pharmacological candidate for mitigating drug\u2010induced nephrotoxicity; however, further studies at the protein and functional levels are warranted.\n                  <\/jats:p>","DOI":"10.1002\/jbt.71055","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T18:38:13Z","timestamp":1785782293000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dexpanthenol Attenuates Methotrexate\u2010Induced Nephrotoxicity Through Modulation of NF\u2010\u03baB\u2013Mediated Inflammation and SIRT1\/PGC\u20101\u03b1\u2013NRF2\/HO\u20101\u2013Associated Oxidative Stress Pathways"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9196-3133","authenticated-orcid":false,"given":"Atila","family":"Altuntas","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Faculty of Medicine Suleyman Demirel University Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1545-035X","authenticated-orcid":false,"given":"Halil","family":"Asci","sequence":"additional","affiliation":[{"name":"Department of Medical Pharmacology, Faculty of Medicine Suleyman Demirel University Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1481-7834","authenticated-orcid":false,"given":"Esma","family":"Selcuk","sequence":"additional","affiliation":[{"name":"Department of Medical Biology, Faculty of Medicine Institute of Health Sciences Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huzeyfe","family":"Karaosman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Faculty of Medicine Suleyman Demirel University Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osman","family":"Aydin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Konya State Hospital Konya T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3739-9580","authenticated-orcid":false,"given":"Ilter","family":"Ilhan","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Faculty of Medicine Suleyman Demirel University Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4586-9298","authenticated-orcid":false,"given":"Sefa Alperen","family":"Ozturk","sequence":"additional","affiliation":[{"name":"Department of Urology, Faculty of Medicine Suleyman Demirel University Isparta T\u00fcrkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1835-1082","authenticated-orcid":false,"given":"Ozlem","family":"Ozmen","sequence":"additional","affiliation":[{"name":"Department of Pathology, Faculty of Veterinary Medicine Burdur Mehmet Akif Ersoy University Burdur 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