ISSN 2149-2263 | E-ISSN 2149-2271
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Myricetin May Improve Cardiac Dysfunction Possibly Through Regulating Blood Pressure and Cellular Stress Molecules in High-Fructose-Fed Rats [Anatol J Cardiol]
Anatol J Cardiol. 2024; 28(1): 55-64 | DOI: 10.14744/AnatolJCardiol.2023.3866

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

Nur Banu Bal1, Ceren Güney2, Onur Gökhan Yıldırım3, Fatma Akar1, Emine Demirel-yılmaz4
1Department of Pharmacology, Faculty of Pharmacy, Gazi University, Ankara, Türkiye
2Department of Pharmacology, Faculty of Pharmacy, Düzce University, Düzce, Türkiye
3Department of Pharmacy Services, Vocational School of Health Services, Artvin Çoruh University, Artvin, Türkiye
4Department of Medical Pharmacology, Faculty of Medicine, Ankara University, Ankara, Türkiye

Background: The aim of this study was to examine the effect of myricetin on cardiac dysfunction 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 acetylcholine 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 acetylcholine-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-κB) and the stress-regulated kinase JNK1, but myricetin only reduced NF-κB 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 irregularities induced by a high-fructose diet through reducing systolic blood pressure, improving cardiac adrenergic responses, suppressing PINK1, NF-κB, and Bax expression, and thus reflecting a potential therapeutic value.

Keywords: Fructose, myricetin, cardiac dysfunction, blood pressure, cellular stress molecules

Nur Banu Bal, Ceren Güney, Onur Gökhan Yıldırım, Fatma Akar, Emine Demirel-yılmaz. Myricetin May Improve Cardiac Dysfunction Possibly Through Regulating Blood Pressure and Cellular Stress Molecules in High-Fructose-Fed Rats. Anatol J Cardiol. 2024; 28(1): 55-64

Corresponding Author: Nur Banu Bal
Manuscript Language: English


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