Fig. 5

Hesperetin slows down cardiac aging in old WT mice. A Representative echocardiography images are shown in different groups of mice (n ≥ 5 per group). B, C Ejection fraction and myocardial performance index obtained from echocardiography analysis. D Representative ECG tracings and continuous 5-min waterfall plots recorded following anesthesia of the mice. Representative dysrhythmic ECGs, namely missing beat, ventricular premature complexes (VPCs), atrioventricular block (AV block), irregular PR interval, and widened QT interval, were found in the old WT mice or Veh-treated mice. E, F QT interval and Tpeak-Tend interval measurements obtained from 5-min sequential beats of whole ECG tracings from baseline. G Cardiac perivascular fibrosis is examined by Sirius Red/Fast Green staining of the hearts with the aim of detecting collagen. H–K TEM analysis reveals ultrastructure of the mitochondria, myofibril, and ICD in the cardiac muscle of young mice at 3-month (H), old WT mice at 24-month (I), Veh-treated WT mice at 24-month (J), and hesperetin-treated WT mice at 24-month (K). Overt ultrastructural abnormalities are present in the cardiac muscles of naturally aged mice or Veh-treated WT mice at 24-month old. Myelin figure (MF); FA, fascia adherens; GJ, gap junction; DS, desmosome; MF, myelin figure; MD, mitochondrial degeneration; myofibril degeneration and disorganization (*). For hesperetin treatment in this study, old WT mice at 21-month old are treated with dietary hesperetin (100 mg/kg/day) or Veh control food for 3 months and sacrificed at 24-month old. Quantified data are presented as mean ± SD and analyzed by one-way ANOVA with Bonferroni multiple comparison test. *p < 0.05; **p < 0.005