Myricetin may improve cardiac dysfunction possibly through regulating blood pressure and cellular stress molecules in high-fructose-fed rats

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dc.contributor.authorBal, Nur Banu
dc.contributor.authorGüney, Ceren
dc.contributor.authorYıldırım, Onur Gökhan
dc.contributor.authorAkar, Fatma
dc.contributor.authorDemirel Yılmaz, Emine
dc.date.accessioned2024-11-15T08:41:51Z
dc.date.available2024-11-15T08:41:51Z
dc.date.issued2024
dc.departmentAÇÜ, Sağlık Hizmetleri Meslek Yüksekokulu, Eczane Hizmetleri Bölümüen_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. High- fructose intake augmented phosphorylation of the proinflammatory molecule Nuclear factor kappa B (NF-?B) and the stress-regulated kinase JNK1, but myricetin only reduced NF-?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-?B, and Bax expression, and thus reflecting a potential therapeutic value.
dc.identifier.doi10.14744/AnatolJCardiol.2023.3866
dc.identifier.endpage64en_US
dc.identifier.issue1en_US
dc.identifier.scopusqualityN/A
dc.identifier.startpage55en_US
dc.identifier.urihttp://dx.doi.org/10.14744/AnatolJCardiol.2023.3866
dc.identifier.urihttps://hdl.handle.net/11494/4948
dc.identifier.volume28en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakTR-Dizin
dc.indekslendigikaynakPubMed
dc.institutionauthorYıldırım, Onur Gökhan
dc.language.isoenen_US
dc.publisherTurkish Society of Cardiologyen_US
dc.relation.ispartofThe Anatolian Journal of Cardiology
dc.relation.publicationcategoryMakale - Ulusal 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.titleMyricetin may improve cardiac dysfunction possibly through regulating blood pressure and cellular stress molecules in high-fructose-fed ratsen_US
dc.typeArticle

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