FIGURE 1.

Reperfusion injury induces cell necroptosis and increases 4-hydroxy-2-non-enal (4-HNE) production in mouse hearts and H9c2 cells. (A,B) Representative photomicrographs and analysis of necrotic area (red) and viable cardiomyocytes (green) in the sections of mouse hearts (n = 6). Scale bar = 100 μm. (C,D) Representative Western blots and relative expression of receptor-interacting serine/threonine-protein kinase 1 (RIP1), p-RIP1, RIP3, p-RIP3, mixed lineage kinase domain-like pseudokinase (MLKL), p-MLKL, Ca²⁺/calmodulin-dependent protein kinase II (CaMKII), and p-CaMKII in mouse hearts (n = 6). (E,F) Representative immunoblots and relative expression of RIP1, p-RIP1, RIP3, and p-RIP3 in H9c2 cells under different reoxygenation times following hypoxia for 14 h (n = 5). (G,H) Protein expression and relative expression of 4-HNE adducts in mouse hearts (n = 6). (I,J) Representative immunohistochemical staining and analysis of mouse heart sections stained with anti-4-HNE antibodies (n = 7). Scale bar = 50 μm. (K,L) Protein expression of 4-HNE adducts in H9c2 cells under different reoxygenation times following hypoxia for 14 h (n = 5). *p < 0.05 vs. sham (control) group; **p < 0.01 vs. sham (control) group.