Nicotinamide adenine dinucleotide inhibits the production of reactive oxygen species and myocardial cell pyroptosis caused by hypoxia/re-oxygenation injury

Figure 2 Assessment of cell viability and apoptosis in H9c2 cells after hypoxia/re-oxygenation injury. A: Live/dead staining of H9c2 cells following hypoxia/re-oxygenation (H/R) treatment, with or without acetylcysteine or nicotinamide adenine dinucleotide oxidized form (NAD⁺) (n = 3); B: Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay results for H9c2 cells subjected to H/R treatment, with or without acetylcysteine or NAD+ (n = 3); C: Reactive oxygen species staining of H9c2 cells after H/R treatment with or without acetylcysteine or NAD⁺ (n = 3). H/R: Hypoxia/re-oxygenation; NAD: Nicotinamide adenine dinucleotide; NAD⁺: Nicotinamide adenine dinucleotide oxidized form.