Fig. 4

Cardiac cell proliferation and angiogenesis following MI with ceAF treatment. a BrdU (green) incorporation in cardiomyocytes from ceAF treated MI mice (n = 6 each). The right image shows a higher magnification image of the boxed region in the left image. Scale bars, 100 μm. b Quantification of the percent of proliferating cardiomyocytes (BrdU+/cTnT+) in control and ceAF treatment group. *, p < 0.05. c Co-immunostaining with anti-PH3 (green) and anti-cTnT (red) of heart tissues in the border zone of infarction 7 days after MI. ceAF treatment showed a significant increase in mitosis of cardiomyocytes in MI mice (n = 6 each). The right image represents the white boxed area in the left image. Scale bar, 100 μm. d Percent of proliferating CMs (PH3+/cTnT+) in response to ceAF treatment. e Co-immunostaining with anti-Ki67 (green) and anti-cTnT (red) of heart tissues in the border zone of infarction 7 days after MI (n = 6). The right image represents the white boxed area in the left image. Scale bar, 100 μm. f Quantification of cells expressing proliferation marker Ki67 in control and ceAF treatment group. *, p < 0.05. g Co-immunostaining with anti-CD31(green) and anti-smooth muscle actin (red) of heart tissues from MI mice treated with 5% glucose or ceAF (n = 4 each). Scale bars, 100 μm. h Vascular density in heart sections of control and ceAF treatment group was quantified by calculating the number of the CD31-positive vascular structures. *, p < 0.05. i Co-immunostaining with anti-CD31 (green) and anti-smooth muscle actin (red) of heart tissues from IR pigs treated with 5% glucose or ceAF (n = 4 each). Scale bars, 100 μm. j Vascular density in heart sections of control and ceAF treatment group. The density was quantified by calculating the number of the CD31-positive vascular structures. *, p < 0.05. Scale bars, 100 μm