Book of Abstracts - New Frontiers 2022

Abstracts of poster presentations

QUERCETIN IMPROVES DIASTOLIC DYSFUNCTION AND REDUCES HEART HYPERTROPHY IN DIABETIC ZDF RATS L. Bartošová 1 , C. Horváth 1 , P. Galis 1 , K. Ferenczyová 2 , B. Kaločayová 2 , A. Szobi 1 , A. Duriš -Adameov á 1,2 , M. Barteková 2,3 , T. Rajtík 1,2 1 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Bratislava, Slovakia; 2 Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovakia; 3 Institute of Physiology, Faculty of Medicine, Comenius University, Bratislava, Slovakia Introduction: Quercetin (QUE) is bioactive flavanol substance with radical scavenging, anti-apoptotic and anti-inflammatory properties both in vitro and in vivo. Its role in diabetes is not sufficiently elucidated, however, hypoglycemic and hypolipidemic activities have been experimentally observed. Nevertheless, there is still lack of information about its role on the heart functions. It has been showed that quercetin potentially inhibits adverse remodeling and improves heart function after myocardial infarction, however, for the type 2 diabetes mellitus (DM2) model such activity was not reported yet. Methods:1-year Zucker Diabetic Fatty male rats were randomized into two groups: non-treated sham animals (Dia) and quercetin-treated animals (DiaQ). As controls male Wistar rats were used, also non treated (C) and quercetin-treated (CQ). QUE was given orally for 6-weeks in dose 20mg/kg/day. Heart functions were measured echocardiographically (GE HealthcareVivid E9) before the onset of the treatment and at the end of experiment. The total level of collagen was measured by hydroxyproline assay and evaluated spectrophotometrically in the tissues of left ventricles (LV). For the protein analysis of remodeling pathways immunoblot analysis was used. Results: QUE-treated animals exhibited decreased E/A wave ratios which suggest improvement of diastolic dysfunction along with reduced intraventricular septum diameter (IVSd) and left ventricular posterior wall (LVPWd) thicknessresulting in reduced overall relative mass thickness (RWT). This effect was further confirmed at the level of total collagen content in LV with significantly decreased collagen in DiaQ when compared to Diahearts. On the protein level myocyte enhancer factor-2 (MEF2) was significantly decreased in DiaQ when compared to Dia group. Conclusions: We have shown that QUE-treatment is capable of improvement of diastolic dysfunction of heart accompanied with overall reduction of ventricular mass. This effect was further supported by decreased collagen content and decreased expression of remodeling-associated transcriptional factor MEF2 in LV, indicating potential anti-remodeling effect of QUE in experimental DM2.

Keywords: quercetin, diabetes mellitus 2, diastolic dysfunction, remodeling

Funding: VEGA 2/0104/20, VEGA 2/0147/18, VEGA 1/0775/21, APVV-18-0548

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