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Chrysin (CHR), a natural flavonoid, possesses significant cytoprotective properties, yet its specific role in mitigating CIP-induced kidney injury remains underexplored. This study investigates the comprehensive nephroprotective mechanisms of CHR against CIP toxicity in rats. Male\n                    <jats:italic>Wistar<\/jats:italic>\n                    rats received CIP (100\u00a0mg\/kg\/day, i.p.) with or without CHR (50\u00a0mg\/kg\/day, p.o.) for 8 consecutive days. Results showed that CIP administration compromised renal function (urea, creatinine) and structural integrity, while markedly altering tubular injury markers (KIM-1, AQP-1). Biochemical and molecular analyses revealed that CIP disrupted cellular redox balance (MDA, GSH, SOD, CAT, GPx) and triggered a robust inflammatory response (NF-\u03baB, TNF-\u03b1, IL-17A). Furthermore, CIP exposure engaged distinct cell death mechanisms, including intrinsic apoptosis (Bax, Bcl-2, Caspase-3) and ferroptosis (GPX4, TfR1, PTGS2). A novel finding was the activation of the Notch signaling pathway (Notch, HES1) in renal tissue. CHR co-treatment significantly attenuated these pathological changes, restoring renal function and histology, re-establishing antioxidant defenses, and suppressing inflammatory and apoptotic signaling and normalizing ferroptosis-related gene expression changes. In conclusion, CHR confers robust nephroprotection by targeting the inflammation-ferroptosis-apoptosis axis and modulating Notch signaling, positioning it as a promising adjuvant to mitigate CIP-induced renal injury.\n                  <\/jats:p>","DOI":"10.1007\/s00210-026-05338-1","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T06:14:27Z","timestamp":1776233667000},"page":"14299-14313","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Chrysin mitigates ciprofloxacin-induced nephrotoxicity: associations with notch\/HES1 signaling, inflammation, and a ferroptosis-related molecular signature"],"prefix":"10.1007","volume":"399","author":[{"given":"Mustafa \u00d6nder","family":"G\u00f6nen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nurhan","family":"Akaras","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hasan","family":"\u015eim\u015fek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00d6zge","family":"Kandemir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00fcneyt","family":"\u00c7a\u011flayan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Serpil","family":"Ayg\u00f6rmez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1930-3293","authenticated-orcid":false,"given":"H\u00fcseyin","family":"Mutlu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatih Mehmet","family":"Kandemir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,15]]},"reference":[{"key":"5338_CR1","doi-asserted-by":"publisher","first-page":"138","DOI":"10.46810\/tdfd.1299663","volume":"12","author":"N Akaras","year":"2023","unstructured":"Akaras N, Kandemir FM, \u015eim\u015fek H, G\u00fcr C, Ayg\u00f6rmez S (2023) Antioxidant, antiinflammatory, and antiapoptotic effects of rutin in spleen toxicity induced by sodium valproate in rats. 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