Hesperidin Attenuates Oxidative Stress, Inflammation, Apoptosis, and Cardiac Dysfunction in Sodium Fluoride-Induced Cardiotoxicity in Rats.


Journal

Cardiovascular toxicology
ISSN: 1559-0259
Titre abrégé: Cardiovasc Toxicol
Pays: United States
ID NLM: 101135818

Informations de publication

Date de publication:
08 2022
Historique:
received: 07 03 2022
accepted: 30 04 2022
pubmed: 24 5 2022
medline: 30 6 2022
entrez: 23 5 2022
Statut: ppublish

Résumé

Excessive 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-κB, IL-1β, TNF-α), 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-κB, IL-1β, TNF-α), 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.

Identifiants

pubmed: 35606666
doi: 10.1007/s12012-022-09751-9
pii: 10.1007/s12012-022-09751-9
doi:

Substances chimiques

Beclin-1 0
NF-kappa B 0
Proto-Oncogene Proteins c-bcl-2 0
Tumor Necrosis Factor-alpha 0
Tumor Suppressor Protein p53 0
bcl-2-Associated X Protein 0
Sodium Fluoride 8ZYQ1474W7
Cytochromes c 9007-43-6
Hesperidin E750O06Y6O
Superoxide Dismutase EC 1.15.1.1
Proto-Oncogene Proteins c-akt EC 2.7.11.1
TOR Serine-Threonine Kinases EC 2.7.11.1
Caspase 3 EC 3.4.22.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

727-735

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Behçet Varışlı (B)

Vocational School of Health Sevices, Final International University, Kazafani, Cyprus.

Ekrem Darendelioğlu (E)

Department of Molecular Biology and Genetics, Faculty of Science and Literature, Bingol University, 12000, Bingol, Turkey.

Cuneyt Caglayan (C)

Department of Biochemistry, Faculty of Veterinary Medicine, Bingol University, 12000, Bingol, Turkey. ccaglayan@bingol.edu.tr.

Fatih Mehmet Kandemir (FM)

Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Turkey. fkandemir03@gmail.com.

Adnan Ayna (A)

Department of Chemistry, Faculty of Science and Literature, Bingol University, 12000, Bingol, Turkey.

Aydın Genç (A)

Department of Biochemistry, Faculty of Veterinary Medicine, Bingol University, 12000, Bingol, Turkey.

Özge Kandemir (Ö)

Technical Sciences Vocatinal School, Aksaray University, Aksaray, Turkey.

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