{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T12:15:15Z","timestamp":1790079315323,"version":"4.0.1"},"reference-count":64,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T00:00:00Z","timestamp":1782345600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T00:00:00Z","timestamp":1782345600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004901","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de Minas Gerais","doi-asserted-by":"publisher","award":["APQ\u201004482\u201024"],"award-info":[{"award-number":["APQ\u201004482\u201024"]}],"id":[{"id":"10.13039\/501100004901","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","award":["001"],"award-info":[{"award-number":["001"]}],"id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Cyclophosphamide is a chemotherapy drug used to treat various types of neoplasms and autoimmune diseases. During its hepatic metabolism, acrolein is formed, a toxic metabolite responsible for increasing oxidative stress in tissues such as the kidney. Acrolein\u2010induced oxidative stress is characterized by the excessive formation of reactive oxygen species (ROS) and lipid peroxidation. Additionally, the release of pro\u2010inflammatory cytokines leads to the accumulation of immune cells in the renal cortex. Therefore, cyclophosphamide\u2010induced nephrotoxicity is a limiting factor in cancer treatment, creating a need to find nephroprotective agents that reduce renal oxidation and inflammation. Nebivolol is a third\u2010generation \u03b2\u2010blocker with established antioxidant effects. This study aimed to evaluate the cytoprotective properties of nebivolol in the renal cortex of mice exposed to cyclophosphamide. Male C57Bl\/6 mice were intraperitoneally injected with a single dose of cyclophosphamide (300\u2009mg\/kg). Nebivolol (10\u2009mg\/kg\/day) was administered by gavage for 5 days prior to cyclophosphamide injection. Nebivolol prevented the cyclophosphamide\u2010induced increase in serum creatinine levels. The cyclophosphamide\u2010induced increases in lipoperoxidation and NADPH oxidase\u2010derived superoxide (O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2022<\/jats:sup>\n                    <jats:sup>\u2212<\/jats:sup>\n                    ) were mitigated by nebivolol. The anti\u2010inflammatory effects of nebivolol included a reduction in the number of neutrophils and macrophages in the renal tissue of cyclophosphamide\u2010treated animals. Finally, nebivolol prevented the cyclophosphamide\u2010induced increase in metalloproteinase (MMP)\u20102 and MMP\u20109 activities. In summary, cyclophosphamide induces renal dysfunction through pro\u2010oxidative and pro\u2010inflammatory mechanisms. Nebivolol exerts nephroprotective effects via antioxidant and anti\u2010inflammatory pathways, preventing cyclophosphamide\u2010induced renal dysfunction. These beneficial effects suggest nebivolol could help prevent the renal toxicity associated with cyclophosphamide.\n                  <\/jats:p>","DOI":"10.1002\/jbt.70996","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T12:35:47Z","timestamp":1782390947000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Nephroprotective Effects of Nebivolol Against Cyclophosphamide\u2010Induced Toxicity Occur via Antioxidant and Anti\u2010Inflammatory Pathways"],"prefix":"10.1002","volume":"40","author":[{"given":"Alessandra O.","family":"Silva","sequence":"first","affiliation":[{"name":"Universidade de S\u00e3o Paulo\u2014USP S\u00e3o Paulo Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo\u00e3o M. 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S.","family":"Jesus","sequence":"additional","affiliation":[{"name":"Universidade de S\u00e3o Paulo\u2014USP S\u00e3o Paulo Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00e9ssyca M.","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Universidade Federal de Alfenas\u2014UNIFAL\u2010MG Alfenas Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jefferson Luiz","family":"Silva","sequence":"additional","affiliation":[{"name":"Universidade do Estado de Minas Gerais\u2014UEMG Belo Horizonte Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V\u00e2nia","family":"Braz\u00e3o","sequence":"additional","affiliation":[{"name":"Universidade de S\u00e3o Paulo\u2014USP S\u00e3o Paulo Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8882-5792","authenticated-orcid":false,"given":"Carla 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