Myricetin May Improve Cardiac Dysfunction Possibly Through Regulating Blood Pressure and Cellular Stress Molecules in High-Fructose-Fed Rats

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dc.authoridGUNEY, Ceren/0000-0002-3267-2886en_US
dc.authorscopusid57190138644en_US
dc.authorscopusid57222266624en_US
dc.authorscopusid56402852700en_US
dc.authorscopusid6701446549en_US
dc.authorscopusid6602268045en_US
dc.contributor.authorBal, Nur Banu
dc.contributor.authorGuney, Ceren
dc.contributor.authorYildirim, Onur Gokhan
dc.contributor.authorAkar, Fatma
dc.contributor.authorDemirel-Yilmaz, Emine
dc.date.accessioned2024-08-23T16:04:01Z
dc.date.available2024-08-23T16:04:01Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractBackground: The aim of this study was to examine the effect of myricetin on cardiac dys- function caused by high fructose intake. Methods: Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. Myricetin was administered by oral gavage for the last 6 weeks. Systolic blood pressure was measured by tail -cuff method. The effects of isoprenaline, phenylephrine, and ace- tylcholine on cardiac contractility and rhythmicity were recorded in the isolated right atrium and left ventricular papillary muscles. In addition to biochemical measurements, the cardiac expressions of cellular stress -related proteins were determined by western blotting. Results: Myricetin improved systolic blood pressure but did not affect body weight, plasma glucose, and triglyceride levels in fructose -fed rats. The impairment of isoprenaline- and phenylephrine-mediated increases in atrial contraction and sinus rate in fructose -fed rats was restored by myricetin treatment. Isoprenaline, phenylephrine, and acetylcho- line -mediated papillary muscle contractions were not changed by fructose or myricetin administration. The expression of the mitochondrial fission marker dynamin-related protein 1 and the mitophagic marker PTEN-induced kinase 1 (PINK1) was enhanced in the fructose -fed rat, and myricetin treatment markedly attenuated PINK1 expression. Highfructose intake augmented phosphorylation of the proinflammatory molecule Nuclear factor kappa B (NF-kappa B) and the stress -regulated kinase JNK1, but myricetin only reduced NF-kappa B expression. Moreover, myricetin diminished the elevation in the expression of the pro-apoptotic Bax. Conclusion: Our results imply that myricetin has a protective role in cardiac irregulari- ties induced by a high -fructose diet through reducing systolic blood pressure, improving cardiac adrenergic responses, suppressing PINK1, NF-kappa B, and Bax expression, and thus reflecting a potential therapeutic value.en_US
dc.description.sponsorshipGazi and Artvin Coruh University Research Fund [TDK-2022- 7661, 2021.S37.02.01]en_US
dc.description.sponsorshipThis study was partially supported by grants from the Gazi and Artvin Coruh University Research Fund (project no: TDK-2022-7661 and 2021.S37.02.01) .en_US
dc.identifier.doi10.14744/AnatolJCardiol.2023.3866
dc.identifier.endpage64en_US
dc.identifier.issn2149-2263
dc.identifier.issn2149-2271
dc.identifier.issue1en_US
dc.identifier.pmid38167793en_US
dc.identifier.scopus2-s2.0-85181577610en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage55en_US
dc.identifier.urihttps://doi.org/10.14744/AnatolJCardiol.2023.3866
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14020
dc.identifier.volume28en_US
dc.identifier.wosWOS:001179772100003en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKare Publen_US
dc.relation.ispartofAnatolian Journal of Cardiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectFructoseen_US
dc.subjectmyricetinen_US
dc.subjectcardiac dysfunctionen_US
dc.subjectblood pressureen_US
dc.subjectcellular stress moleculesen_US
dc.subjectMetabolic Syndromeen_US
dc.subjectMapken_US
dc.subjectHypertensionen_US
dc.titleMyricetin May Improve Cardiac Dysfunction Possibly Through Regulating Blood Pressure and Cellular Stress Molecules in High-Fructose-Fed Ratsen_US
dc.typeArticleen_US

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