作者: He Wang , Xiaoping Liang , Guoan Luo , Mingyu Ding , Qionglin Liang
DOI: 10.1039/C6MB00108D
关键词: Nicotinamide adenine dinucleotide 、 Nicotinamide 、 NAD+ kinase 、 Succinate dehydrogenase 、 Heart metabolism 、 Reactive oxygen species 、 Biology 、 Mitochondrion 、 Pharmacology 、 Biochemistry 、 Metabolism
摘要: Hypoxia/re-oxygenation (H/R) injury is an important cause of heart failure and results in a critical metabolism dysfunction. In this paper, the cytoprotective effect nicotinamide adenine dinucleotide (NAD) precursor was evaluated using vitro model cardiac H/R injury. Nicotinamide (0-20 mM) applied to myoblast cell line H9c2 which subjected hypoxia (12, 24, 36 h) followed by re-oxygenation process (0, 4, 8, 12 h). Cell viability measured, mitochondrial metabolites were extracted then measured HPLC/MS/MS. The present study showed that could down-regulate NADH/NAD ratio maintain NAD-dependent processes. Furthermore, aberrant decrease fumarate levels increase succinate observed group, demonstrated be caused nicotinamide-induced dehydrogenase (SDH) inhibition. These suggest exerts protective on cardiomyoblasts against H/R-induced through both regulation reduction reactive oxygen species generation via SDH