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. 2020 Mar 25;12(6):5362–5383. doi: 10.18632/aging.102956

Figure 2.

Figure 2

Delphinidin attenuated cardiac hypertrophy and improved cardiac function induced by pressure overload in vivo. (A) Statistical differences in the heart weight/body weight (HW/BW) and heart weight/tibia length (HW/TL) ratios between sham and TAC mice treated with vehicle or delphinidin (n=8). (B) Echocardiographic parameters in sham and TAC mice treated with vehicle or delphinidin (n=8). (C) Left, Hematoxylin-eosin (H&E) staining was performed to assess hypertrophic growth of the hearts of sham and TAC mice treated with vehicle or delphinidin (n=8). Right, Statistical analysis of differences in cardiomyocyte size (n=8). (D) Quantitative dihydroethidium (DHE) staining (n=8). (E) Chemiluminescence lucigenin assay (n=8). (F) Quantitative real-time PCR (qRT-PCR) was performed to analyze the mRNA levels of hypertrophic genes (n=5). In A–E, **p<0.01 versus the sham group; ***p<0.001 versus the sham group; ns versus the TAC group; #p<0.05 versus the TAC group; ##p<0.01 versus the TAC group; ###p<0.001 versus the TAC group. qRT-PCR was performed to analyze the mRNA levels of hypertrophic genes (n=5). In A–E, **p<0.01 versus the sham group; ***p<0.001 versus the sham group; ns versus the TAC group; #p<0.05 versus the TAC group; ##p<0.01 versus the TAC group; ###p<0.001 versus the TAC group.