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. 2020 Jul 30;11(7):599. doi: 10.1038/s41419-020-02805-2

Fig. 1. α-LA attenuates TAC-induced LV hypertrophy and heart failure in wild-type mice.

Fig. 1

a Quantitative analysis of heart-to-body weight ratio (HW/BW) (n = 8–10 mice per group); b Quantitative analysis of lung-to-body weight ratio (LW/BW) (n = 8–10 mice per group); c left ventricular ejection fraction (LVEF, %) (n = 8–10 mice per group); d left ventricular fractional shortening (LVFS, %) (n = 8–10 mice per group); e hematoxylin-eosin (H&E, scale bar = 2 mm) staining; f wheat germ agglutinin (WGA, scale bar = 50 μm) staining; g quantitative analysis of cardiomyocyte cross-sectional areas (CSA) (n = 7–15 mice per group); h cardiomyocyte peak shortening (PS, normalized to resting cell length) (n = 300 cells per group); i maximal velocity of shortening (+dL/dt) (n = 300 cells per group); j maximal velocity of relengthening (−dL/dt) (n = 300 cells per group); k time-to-90% relengthening (TR90) in isolated cardiomyocytes (n = 300 cells per group). Mean ± SEM, *P < 0.05, **P < 0.01, ****P < 0.0001. Statistical analysis was carried out by a one-way ANOVA analysis followed by Tukey’s test for post hoc analysis.