Research Paper Volume 12, Issue 6 pp 5362—5383

Delphinidin attenuates pathological cardiac hypertrophy via the AMPK/NOX/MAPK signaling pathway

Figure 6. Compound C abrogated the effects of delphinidin on Ang II-induced cardiomyocyte hypertrophy and oxidative stress by blocking AMPK activity. (A) NRCMs were treated with Ang II (1 μM) for 24 hours in the presence of delphinidin (50 μM) or compound C. α-Actinin staining was performed to determine cell size. Representative images (A1) and quantified cell sizes (A2) of each group are shown (scale bar=20 μm). Cell surface areas (μm2) were measured in 3 independent experiments with at least 100 cells counted for each condition. (B) qRT-PCR was performed to analyze the expression of hypertrophic genes. (C, D), Representative image and quantitative analysis of ROS generation measured by DCF-DA and DHE staining. (E) Statistical analysis of differences in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. A.U., arbitrary units. In AE, *p<0.05 versus the Ang II group; **p<0.01 versus the Ang II group; ***p<0.001 versus the Ang II group; #p<0.05 versus the Ang II+Dp group; ##p<0.01 versus the Ang II+Dp group; ###p<0.001 versus the Ang II+Dp group.