Kankılıç, Nazım AbdülkadirŞimşek, HasanAkaras, NurhanGür, CihanKüçükler, SefaGencer, SelmanKandemir, Fatih Mehmet2024-07-022024-07-0220240278-6915https:/dx.doi.org/10.1016/j.fct.2024.114791https://hdl.handle.net/20.500.12451/12006Bortezomib is a proteasome inhibitor antineoplastic agent that was the first to be approved for cancer treatment. One of bortezomib's most prominent dose-limiting effects is nephrotoxicity; the underlying mechanism is believed to be oxidative stress. Chrysin is a compound found actively in honey and many plant species and stands out with its antioxidant properties. The present study aimed to determine the ameliorative effects of chrysin in bortezomib-induced nephrotoxicity. Material-method: Thirty-five male Wistar rats were divided into control, BTZ, CHR, BTZ + CHR25, and BTZ + CHR50. Biochemical, molecular, Western blot, and histological methods analyzed renal function indicators, oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and damage pathways. Results: Chrysin decreased oxidative stress by reducing oxidants (MDA) and increasing antioxidants (SOD, CAT, Gpx, GSH, Nrf-2, HO-1, NQO1). Chrysin reduced endoplasmic reticulum stress by decreasing ATF-6, PERK, IRE1, and GRP-78 levels. Chrysin reduced inflammation damage by inhibiting the NF-?B pathway. Chrysin exhibited protective properties against apoptotic damage by decreasing Bax and Caspase-3 levels and increasing Bcl-2 levels. In addition, chrysin improved renal function and structural integrity and exhibited healing properties against toxic damage in tissue structure. Conclusion: Overall, chrysin exhibited an ameliorative effect against bortezomib-induced nephrotoxicity.eninfo:eu-repo/semantics/embargoedAccessApoptosisBortezomibChrysinInflammationNephrotoxicityOxidative stresArticle190-10.1016/j.fct.2024.114791Q1N/A