Hesperidin ameliorates vancomycin-induced kidney injury via multipathway modulation: Nrf-2/HO-1, Caspase-3/Bax/Bcl-2, ATF-4, KIM-1 and improved renal tissue function

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dc.authorid0000-0003-3936-4146
dc.contributor.authorGencer, Selman
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Özge
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorKankılıç, Nazım Abdülkadir
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-07-17T08:44:34Z
dc.date.available2025-07-17T08:44:34Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractVancomycin (VCM) is a therapeutic agent used to treat drug-resistant gram-positive bacteria. However, its high-dose use is associated with nephrotoxicity, limiting its clinical application. Hesperidin (HES), a flavonoid naturally found in citrus fruits, exhibits various biological and pharmacological activities, including anti-inflammatory, antioxidant, and anticancer effects. While HES has been shown to exert protective effects in several organ systems, its potential role in preventing VCM-induced nephrotoxicity remains unclear. This study investigates whether HES can mitigate VCM-induced renal damage through its antioxidant and anti-inflammatory properties. VCM was administered intraperitoneally at a dose of 200 mg/kg for seven days. HES (100 mg/kg and 200 mg/kg) was administered orally for seven days. Biochemical, and molecular methods were used to investigate indicators of oxidative stress, ER stress damage, apoptotic and autophagic death in kidney tissue. Additionally, histological methods were used to determine the structural and functional characteristics of kidney tissue. HES treatment alleviated VCM-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased MDA levels, a marker of lipid peroxidation. In addition, HES increased antioxidant activity by activating the Nrf2 signaling pathway. VCM-induced increases in apoptotic Bax, Caspase-3, and P53 were reduced by HES, while the decreased level of antiapoptotic Bcl-2 was increased. HES reduced VCM-induced ER stress damage by reducing the levels of ATF-4, ATF-6, eIF2-α, and CHOP. HES treatment attempted to preserve kidney function and structural integrity. Overall, HES was effective in reducing VCM-induced nephrotoxicity damage and may be an effective treatment option.
dc.identifier.doi10.1016/j.bcp.2025.117131
dc.identifier.issn00062952
dc.identifier.scopus105009758554
dc.identifier.urihttps://dx.doi.org/10.1016/j.bcp.2025.117131
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13349
dc.identifier.volume240
dc.indekslendigikaynakScopus
dc.institutionauthorKaraca, Onur
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorKandemir, Özge
dc.institutionauthorKandemir, Fatih Mehmet
dc.institutionauthorKankılıç, Nazım Abdülkadir
dc.language.isoen
dc.publisherElsevier Inc.
dc.relation.ispartofBiochemical Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectER stress
dc.subjectHesperidin
dc.subjectVancomycin
dc.titleHesperidin ameliorates vancomycin-induced kidney injury via multipathway modulation: Nrf-2/HO-1, Caspase-3/Bax/Bcl-2, ATF-4, KIM-1 and improved renal tissue function
dc.typeArticle

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