| Autor: |
Bartošová, Linda, Horváth, Csaba, Galis, Peter, Ferenczyová, Kristína, Kaločayová, Barbora, Szobi, Adrián, Duriš-Adameová, Adriana, Barteková, Monika, Rajtík, Tomáš |
| Předmět: |
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| Zdroj: |
European Pharmaceutical Journal; 2022 Supplement, Vol. 69, p31-31, 1p |
| Abstrakt: |
Quercetin (QUE) is a widely known polyphenolic flavonoid that possesses a notable antioxidative, anti-inflammatory, and antiapoptotic activities that were also recorded by multiple studies on cardiovascular pathologies. Therefore, it is rational to employ QUE in a study that comprises both diabetes mellitus 2 (DM2) and obesity as a base for cardiovascular disease development, given that such an experimental model has not been explored yet. The exact role of QUE in either DM2 or cardiac remodelling remains elusive, even though published reports suggest a protective role of QUE against heart remodelling or diabetes. In this study, 1-year-old male Zucker diabetic fatty rats were randomised into two groups: nontreated sham (Dia) and QUEtreated (DiaQ). Wistar rats were used as control groups: nontreated (C) and QUE-treated (CQ) groups. QUE treatment was administered orally at a dose of 20 mg/kg/day for 6 weeks. Echocardiography (GE Healthcare Vivid E9) was performed to assess heart parameters before the onset of treatment and at the end of the experiment. Hydroxyproline assay was used to measure total levels of collagen in left ventricles (LVs) and protein content was analysed by western blot. QUE normalised E/A ratio in the DiaQ group, which indicates an improvement of diastolic dysfunction. Moreover, QUE reduced interventricular septum diameter and left ventricular posterior wall thickness, resulting in reduced relative wall thickness. Similarly, total LV collagen content was decreased in the DiaQ group compared to the Dia group. Furthermore, protein level of myocyte enhancer factor-2 (MEF2) was significantly decreased in the DiaQ group when compared to the Dia group. QUE treatment alleviated diastolic dysfunction of the heart accompanied by an overall reduction of ventricular mass and collagen content in LV. This observation was further supported by decreased expression of remodelling-associated MEF2. Our results indicate that QUE might exert potential cardioprotective and antiremodelling effects in experimental DM2. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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