Boric acid mitigates alcohol-induced renal podocyte injury, apoptosis, and oxidative stress in HBV transgenic mice

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dc.authorid0000-0001-8250-8227
dc.authorid0009-0006-6939-4054
dc.authorid0000-0002-1173-7759
dc.authorid0000-0001-7243-3671
dc.authorid0000-0003-3194-9676
dc.authorid0000-0001-6032-3328
dc.authorid0000-0002-5757-1256
dc.authorid0000-0001-7724-6488
dc.contributor.authorŞevgin, Kübra
dc.contributor.authorErgüven, Pelin
dc.contributor.authorTanrıkulu Küçük, Sevda
dc.contributor.authorDeğirmencioğlu, Sevgin
dc.contributor.authorÇetinalp, Pınar
dc.contributor.authorAksu, Soner
dc.contributor.authorGün Atak, Palmet
dc.contributor.authorSöğüt, İbrahim
dc.date.accessioned2026-03-25T13:41:56Z
dc.date.available2026-03-25T13:41:56Z
dc.date.issued2026
dc.departmentFakülteler, Mühendislik ve Doğa Bilimleri Fakültesi, Moleküler Biyoloji ve Genetik Bölümü
dc.description.abstractChronic alcohol consumption exacerbates kidney injury, particularly in individuals with hepatitis B virus (HBV) infection. This study investigated the protective effects of boric acid supplementation against alcohol-induced renal damage in HBV transgenic mice. HBV transgenic mice were divided into four groups: control (C), boric acid (B), alcohol (A), and alcohol + boric acid (A + B). Renal injury was evaluated using H&E, PAS, TUNEL, and desmin staining. The expression of caspase-3, cytochrome c, and APAF-1 was analyzed by qRT-PCR. Biochemical analyses included BUN, creatinine, oxidative stress markers (ROS, MDA, TOS, OSI), total antioxidant status, and antioxidant enzyme activities (SOD, CAT, GPx). Histopathological findings showed activated parietal epithelial cells in all groups, indicating renal injury. Alcohol significantly increased tubular damage, podocyte desmin expression, apoptosis, cytochrome c and APAF-1 mRNA levels, and oxidative stress markers, while reducing antioxidant enzyme activities and BUN levels compared with controls. Boric acid supplementation significantly mitigated alcohol-induced tubular injury, apoptosis, oxidative stress, and serum creatinine levels, and improved BUN values. Boric acid treatment alone also alleviated glomerular and tubular injury and reduced tubular apoptosis compared with HBV control mice. Overall, boric acid exerts renoprotective effects in HBV-transgenic mice subjected to chronic alcohol exposure by inhibiting oxidative stress, apoptosis, and podocyte injury.
dc.identifier.citationŞevgin, K., Ergüven, P., Tanrıkulu Küçük, S., Değirmencioğlu, S., Çetinalp, P., Aksu, S., Gün Atak, P., & Söğüt, İ. (2026). Boric acid mitigates alcohol-induced renal podocyte injury, apoptosis, and oxidative stress in HBV transgenic mice. Antioxidants, 15(3), pp. 1-14. https://doi.org/10.3390/antiox15030318
dc.identifier.doi10.3390/antiox15030318
dc.identifier.endpage14
dc.identifier.issn2076-3921
dc.identifier.issue3
dc.identifier.scopusqualityQ1
dc.identifier.startpage1
dc.identifier.urihttps://doi.org/10.3390/antiox15030318
dc.identifier.urihttps://hdl.handle.net/20.500.13055/1369
dc.identifier.volume15
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.indekslendigikaynak.otherSCI-E - Science Citation Index Expanded
dc.institutionauthorAksu, Soner
dc.institutionauthorid0000-0001-6032-3328
dc.language.isoen
dc.publisherMDPI Publishing
dc.relation.ispartofAntioxidants
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectBoric Acids
dc.subjectKidney
dc.subjectOxidative Stress
dc.titleBoric acid mitigates alcohol-induced renal podocyte injury, apoptosis, and oxidative stress in HBV transgenic mice
dc.typeArticle
dspace.entity.typePublication

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