NAD (sodium)

NAD sodium is an orally effective cofactor and homeostatic regulator. NAD sodium can be reduced to β-nicotinamide adenine dinucleotide (NADH) during coupling with reactions that oxidize organic substrates. NAD sodium can be converted to β-nicotinamide adenine dinucleotide (NADH) and passes to the inside of mitochondria, which indirectly generates ATP. NAD sodium can be used for the research of non-alcoholic fatty liver disease, obesity, and glucose intolerance^{[1][2][3][4][5]}. In Vitro:NAD (sodium) (250 pM, 100 μM; 5-60 min, 10 min) is transported into NIH-3T3 cells with an apparent K_m of ~190 μM, and co-treatment with unlabeled NAD competes for transport^[4].
NAD (sodium) (100 μM; 72 h) rescues FK866-induced cell death and replenishes intracellular NAD(P) levels in NIH-3T3 cells^[4].
NAD (sodium) (250 pM; 10 min) is transported into SH-SY5Y, HeLa, HaCaT, HMEC, and RAW 264.7 cells but not K562 cells, with sodium-dependent transport in SH-SY5Y cells^[4].
NAD (sodium) (100 μM; 72 h) rescues FK866-induced cell death and replenishes intracellular NAD(P) levels in SH-SY5Y cells^[4].
NAD (sodium) (100 μM; 36 h) reverts FK866-induced autophagy in SH-SY5Y cells^[4].
NAD (sodium) (0.5 mM) promotes M2 macrophage polarization and inhibits M1 macrophage polarization in both normal and high glucose-exposed RAW264.7 cells^[5].
NAD (sodium) (0.5 mM; 24 h) restores reduced VEGF secretion in high glucose-exposed mouse bone marrow-derived macrophages^[5].
NAD (sodium) (0.5 mM; 24 h) modulates BMDM to secrete factors that restore HUVEC tube formation, migration, and scratch wound closure impaired by high glucose exposure^[5].
NAD (sodium) (0.5 mM) promotes pro-angiogenic VEGF165 expression and inhibits anti-angiogenic VEGF165b expression in both normal and high glucose-exposed RAW264.7 cells^[5].
NAD (sodium) (0.5 mM) restores reduced SRSF1 expression and inhibits increased SRSF6 expression in high glucose-exposed RAW264.7 cells, and modulates these splicing factors in normal glucose cells^[5].
NAD (sodium) (0.5 mM; 24 h) reverses impaired HUVEC scratch wound closure caused by conditioned medium from NAD⁺-depleted RAW264.7 cells^[5].
NAD (sodium) (0.5 mM) restores reduced pro-angiogenic VEGF165 expression and inhibits increased anti-angiogenic VEGF165b expression in NAD⁺-depleted RAW264.7 cells^[5]. In Vivo:NAD⁺ (500 mg/kg/day; i.p.; daily; at least 28 days) attenuates cardiac injury and improves cardiac function after myocardial infarction in both diabetic and non-diabetic mice by restoring cardiac NAD⁺ levels, reducing infarct size, promoting M2 macrophage polarization, and enhancing angiogenesis, while also lowering blood glucose in diabetic mice^[5].