©The Author(s) 2026.
World J Cardiol. Jan 26, 2026; 18(1): 114108
Published online Jan 26, 2026. doi: 10.4330/wjc.v18.i1.114108
Published online Jan 26, 2026. doi: 10.4330/wjc.v18.i1.114108
Figure 3 Measurement of total cellular nicotinamide adenine dinucleotide levels and the nicotinamide adenine dinucleotide oxidized form/nicotinamide adenine dinucleotide reduced form ratio in H9c2 cells after hypoxia/re-oxygenation treatment, with or without ace tylcysteine or nicotinamide adenine dinucleotide oxidized form (n = 4).
A and B: The normal group refers to H9c2 cells cultured in an incubator containing 21% oxygen and 5% CO2, and serves as the control group; the hypoxia/re-oxygenation (H/R) group refers to H9c2 cells subjected to H/R; the H/R + acetyl group refers to H9c2 cells cultured under an H/R procedure with acetylcysteine treatment; the H/R + nicotinamide adenine dinucleotide group refers to H9c2 cells cultured under an H/R procedure with nicotinamide adenine dinucleotide oxidized form (NAD+) treatment. H/R: Hypoxia/re-oxygenation; NAD: Nicotinamide adenine dinucleotide; NAD+: Nicotinamide adenine dinucleotide oxidized form; NADH: Nicotinamide adenine dinucleotide reduced form.
- Citation: Dong S, Liu YQ, Tu YJ, Gao S, Liu YJ, Liu C, Pei ZW. Nicotinamide adenine dinucleotide inhibits the production of reactive oxygen species and myocardial cell pyroptosis caused by hypoxia/re-oxygenation injury. World J Cardiol 2026; 18(1): 114108
- URL: https://www.wjgnet.com/1949-8462/full/v18/i1/114108.htm
- DOI: https://dx.doi.org/10.4330/wjc.v18.i1.114108