NAD+ (β-Nicotinamide Adenine Dinucleotide) is a coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH).

METHODS: HEK293 cells were treated with FK866 (2 µM) and NAD+ (100 µM) for 48 h. Metabolic activity was determined by MTT Assay.
RESULTS: Addition of FK866 to the culture medium resulted in rapid depletion of intracellular NAD stores and inhibition of the metabolic activity of NADPH-dependent dehydrogenase. When supplemented with additional NAD+, the metabolic activity of the cells returned to control levels. [1]
METHODS: Isolated microvessels from rat retina were treated with NAD+ (0-1000 nM) for 0-24 h. Cell death was detected using trypan blue dye.
RESULTS: Exposure to NAD+ increased microvascular cell death in a dose-dependent manner, with the half-maximum effective concentration of NAD+ being approximately 2 nM. assessment of the time course of NAD+-induced vascular toxicity showed that cell death was detected after 16 h of NAD+ exposure. [2]

METHODS: To study the effects on ischemia/reperfusion (I/R) injury, NAD+ (5-20 mg/kg) was injected intravenously into Wistar rats with myocardial ischemia/reperfusion.
RESULTS: Injections of 10-20 mg/kg NAD+ dose-dependently reduced I/R-induced myocardial infarction, with a dose of 20 mg/kg NAD+ reducing infarction by approximately 85%. Injection of NAD+ significantly reduced I/R-induced apoptotic cardiac injury. [3]