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. 2018 Jul 12;7(14):e005171. doi: 10.1161/JAHA.116.005171

Figure 7.

Figure 7

CCK2R antagonist CI988 abolished the gastrin‐mediated protective effect against I/R‐injury. The protective effect of gastrin was assessed in a Langendorff‐perfused system in the presence and absence of CI988. The cTnI concentration (A) was measured using an autoanalyzer, and LDH concentration (B) was measured by ELISA. Cardiomyocyte apoptosis was determined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick‐end labeling) assay (C) and caspase 3 activity (D). Cardiac infarct size was measured by triphenyltetrazolium chloride staining (E). Phosphorylation of ERK1/2 (F), AKT (G), and STAT3 (H) was determined by immunoblotting. *P<0.01 vs I/R, # P<0.01 vs gastrin+I/R, 1‐way ANOVA, Holm–Sidak test, n=8 per group. AKT indicates protein kinase B; CCK2R, cholecystokinin 2 receptor; cTnI indicates cardiac troponin I; ERK1/2, extracellular signal‐regulated kinase 1/2; gastrin+I/R, intraperitoneal injection of gastrin before ischemia/reperfusion; I/R indicates ischemia/reperfusion; LDH, lactate dehydrogenase; LV, left ventricle; p, phosphorylated; STAT3, signal transducer and activator of transcription 3; t, total.