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

Figure 6.

Figure 6

Role of RISK and SAFE pathways in mediating the protective effects of gastrin on I/R‐injured heart in a Langendorff perfusion system. The protective effect of gastrin on I/R‐injured heart was investigated with or without the presence of specific inhibitors. These inhibitors included PD98095 (ERK1/2 inhibitor), LY294002 (AKT inhibitor), and S3I‐201 (STAT3 inhibitor). The concentrations of cTnI (A) and LDH (B) in coronary effluent, number of TUNEL (terminal deoxynucleotidyl transferase dUTP nick‐end labeling)–positive cells (C), caspase 3 activity (D), and infarct size of heart (E) were detected in all groups at the end of reperfusion. *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; 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.