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

Figure 8.

Figure 8

Gastrin attenuated I/R‐induced myocardial damage in in vivo experiments. The protective effect of gastrin was confirmed in an in vivo I/R model. These parameters included plasma cTnI (A) and LDH (B) concentrations, cardiac apoptosis determined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick‐end labeling) assay (C) and caspase 3 activity (D), and infarct size (E). The protective effects of gastrin against I/R injury were assessed in the presence and absence of CI988, a CCK2R antagonist. CI988 blocked the gastrin‐induced RISK and SAFE activation in I/R‐treated rat heart. The protective effect of gastrin was assessed in I/R‐treated rat heart in the presence and absence of CI988. RISK and SAFE activation is shown as phosphorylation of ERK1/2 (F), AKT (G), and STAT3 (H) in I/R‐treated rat heart. *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; RISK, reperfusion injury salvage kinase; SAFE, survivor activating factor enhancement; STAT3, signal transducer and activator of transcription 3.