Research Paper Volume 12, Issue 6 pp 5362—5383

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

Figure 4. Delphinidin inhibited Ang II-induced hypertrophy in NRCMs. (A) The Cell Counting Kit-8 assay was used to detect the cell viability of cardiomyocytes treated with different concentrations of delphinidin (n=4). (B) NRCMs were treated with Ang II (1 μM) for 24 hours in the presence of delphinidin (10 and 50 μM) or DMSO. α-Actinin staining was performed to determine cell size. Representative images (left) and quantified cell sizes (right) 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. (C) qRT-PCR was performed to analyze the expression of hypertrophic genes. (D and E) Representative image and results of quantitative analysis of ROS generation measured by DCF-DA and DHE staining. (F) Statistical analysis of differences in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. A.U., arbitrary units. In AF,**p<0.01 versus the control group; ***p<0.001 versus the control group; ns versus the Ang II group; #p<0.05 versus the Ang II group; ##p<0.01 versus the Ang II group; ###p<0.001 versus the Ang II group.