Key result
Quercetin shortens myocardial relaxation time by ~11% in isolated ventricles from diabetic mice.
Why the study?
The effect of quercetin on myocardial relaxation in normal and diabetic ventricular myocardium was investigated to understand its lusitropic properties.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for quercetin in diabetic diastolic dysfunction; requires in vivo and clinical validation before any therapeutic consideration.
The lusitropic effect of quercetin was examined on isolated ventricular myocardial tissue preparations from normal and streptozotocin-induced diabetic mice. The time required for 90% relaxation of the myocardium, which was prolonged in the diabetic mice, was shortened by quercetin in both normal and diabetic myocardia. This effect of quercetin was completely inhibited by cyclopiazonic acid but not by SEA0400. These results indicated that quercetin accelerates myocardial relaxation through activation of the sarco–endoplasmic reticulum Ca2+-ATPase.
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Hamaguchi et al. (2021) studied Streptozotocin-induced diabetes mellitus (n=36). Quercetin vs. Baseline (before application) was evaluated on Time required for 90% relaxation of the myocardium (relaxation time) in diabetic mice (MD -8.6 ms, p=<0.001). Quercetin at 30 µM shortened the prolonged myocardial relaxation time in isolated ventricular preparations from diabetic mice from 78.1 ms to 69.5 ms.
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