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However, Hb treatment, a NO scavenger, reversed the above myocardial protective effects of VS-1. In the C-Hb group, cardiomyocyte apoptosis was increased again to the level of the C-Ad-Null group. In the T-Hb group, although cardiomyocyte apoptosis was also increased, it was still significantly CB-839 cost lower than in the T-Ad-Null group (Figure 2). AST and CK-MB, cardiac cell-specific enzymes, levels are elevated upon the damage of myocardial cells (Francis et al., 2012; Prabodh et al., 2012). As expected, the levels of AST (Figure 3A) and CK-MB (Figure 3B) in T-Ad-null group were significantly increased compared with the C-Ad-null group (P?Ritipenem group, but partially suppressed by Hb in the T-Hb group. Myocardial apoptosis in groups of endothelial cell-mediated cardiomyocytes treated with H/R (Figure 4) was measured at the end of the experiment. After stimulation of H/R, apoptosis in cardiomyocytes in the Ad-null group was 6.8?��?0.2%. This was reduced to 3.9?��?0.12% in the Ad-VS-1 group, which was significantly less than in the Ad-null group (P?Volasertib mouse gene transfection significantly decreased their expression. But Hb eliminated the above protective effects of VS-1 on the levels of AST and CK-MB, leading to their high levels (Figure 5). Kuramochi et al. (2004) found that mixed culture of endothelial cells and myocardial cells inhibited oxygen free radical-induced apoptosis in myocardial cells, and helped to coordinate and couple the synchronization between systolic and diastolic myocardial cells. In addition, myocardial cells provided a feedback to secrete cytokines (such as vascular endothelial growth factor, VEGF) that affected the function of endothelial cells. In examining the protection of endothelial cells on myocardial cells, we have shown that, compared with the cardiomyocytes alone culture group, cardiomyocyte injury was more serious in the presence of endothelial cells with higher levels pf apoptosis, AST, and CK-MB, which indicates that damage products (including oxygen free radicals, inflammatory cytokines, and lysosomal degradation pathway) may be exchanged between endothelial cells and myocardial cells, resulting in the injury being superimposed.