Fig. 6.

CCK₂R role in the protective effects of gastrin against myocardial infarction. Endothelial cells were treated with gastrin (100 nM) with or without the CCK₂R inhibitor, CI988 (100 nM). a Western blot was used to detect the protein levels of vascular endothelial growth factor (VEGFA). Results are expressed as the ratio of VEGFA to GAPDH. n = 4. ^*P < 0.05, vs. Control; ^#P < 0.05, vs. gastrin-treated group. b Representative images and quantification of endothelial cell tube formation assay in vitro. Scale bar = 50 µm. n = 4. ^*P < 0.05, vs. Control; ^#P < 0.05, vs gastrin-treated group. Myocardial infarction mice were infused with gastrin or/and CI988. c1 Immunofluorescence staining with anti-cluster of differentiation 31 (CD31) antibody showed the microvessel densities in the infarcted border zone 14 days after MI. DAPI is blue, and CD31 is red. Scale bar = 50 µm. c2 Western blot was used to detect the protein levels of CD31 in the peri-infarct area of the heart 14 days after MI. Results are expressed as the ratio of CD31 to GAPDH. n = 8. ^*P < 0.05, vs. MI group; ^#P < 0.05, vs gastrin-treated MI mice. d1 Representative M-mode images of hearts with MI 28 days after gastrin or/and CI988 infusion. d2–3 Left ventricle ejection fraction (EF), fractional shortening (FS) 7, 14, and 28 days after MI. n = 8. ^*P < 0.05, vs. MI + Gastrin + CI988