Hesperidin attenuates oxidative stress, inflammation, apoptosis, and cardiac dysfunction in sodium fluoride?Induced cardiotoxicity in rats

Basit Öğe Kaydı
dc.authorid0000-0001-5608-554X
dc.contributor.authorVarışlı, Behçet
dc.contributor.authorDarendelioğlu, Ekrem
dc.contributor.authorÇağlayan, Cüneyt
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorAyna, Adnan
dc.contributor.authorGenç, Aydın
dc.contributor.authorKandemir, Özge
dc.date.accessioned2022-06-17T07:29:00Z
dc.date.available2022-06-17T07:29:00Z
dc.date.issued2022
dc.departmentTıp Fakültesi
dc.description.abstractExcessive fluoride intake has been reported to cause toxicities to brain, thyroid, kidney, liver and testis tissues. Hesperidin (HSP) is an antioxidant that possesses anti-allergenic, anti-carcinogenic, anti-oxidant and anti-inflammatory activities. Presently, the studies focusing on the toxic effects of sodium fluoride (NaF) on heart tissue at biochemical and molecular level are limited. This study was designed to evaluate the ameliorative effects of HSP on toxicity of NaF on the heart of rats in vivo by observing the alterations in oxidative injury markers (MDA, SOD, CAT, GPX and GSH), pro-inflammatory markers (NF-?B, IL-1?, TNF-?), expressions of apoptotic genes (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic markers (Beclin 1, LC3A, LC3B), expression levels of PI3K/Akt/mTOR and cardiac markers. HSP treatment attenuated the NaF-induced heart tissue injury by increasing activities of SOD, CAT and GPx and levels of GSH, and suppressing lipid peroxidation. In addition, HSP reversed the changes in expression of apoptotic (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic and inflammatory parameters (Beclin 1, LC3A, LC3B, NF-?B, IL-1?, TNF-?), in the NaF-induced cardiotoxicity. HSP also modulated the gene expression levels of PI3K/Akt/mTOR signaling pathway and levels of cardiac markers (LDH, CK-MB). Overall, these findings reveal that HSP treatment can be used for the treatment of NaF-induced cardiotoxicity.
dc.identifier.doi10.1007/s12012-022-09751-9
dc.identifier.endpage-en_US
dc.identifier.issn1530-7905
dc.identifier.issue-en_US
dc.identifier.pmid35606666
dc.identifier.scopusqualityQ1
dc.identifier.startpage-en_US
dc.identifier.urihttps:/dx.doi.org/10.1007/s12012-022-09751-9
dc.identifier.urihttps://hdl.handle.net/20.500.12451/9433
dc.identifier.volume-en_US
dc.identifier.wosWOS:000799064400001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofCardiovascular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectCardiotoxicity
dc.subjectHesperidin
dc.subjectOxidative Stress
dc.subjectSodium Fluoride
dc.titleHesperidin attenuates oxidative stress, inflammation, apoptosis, and cardiac dysfunction in sodium fluoride?Induced cardiotoxicity in rats
dc.typeArticle

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