β-nicotinamide mononucleotide (NMN) is a natural nucleotide and a key intermediate in the synthesis of coenzyme I (NAD+). β-nicotinamide mononucleotide is involved in a number of biochemical reactions in the human body, which are related to immunity and metabolism.

METHODS: Human corneal epithelial cells HCECs were treated with glucose (25 mM) and β-nicotinamide mononucleotide (5-1000 µM) for 48 h. Cell viability was measured by Trypan blue staining.
RESULTS: The effects of different concentrations of β-nicotinamide mononucleotide on HCEC damage induced by high glucose were analyzed. 125, 250 and 500 µM β-nicotinamide mononucleotide showed significant protective effects. [1]
METHODS: Late passaged MSCs LP MSCs were treated with β-nicotinamide mononucleotide (100 µM) for 24 h and mitochondrial morphology was analyzed.
RESULTS: The mitochondrial staining in LP-MSCs was more diffuse and less intense, while the distribution of mitochondria became concentrated after β-nicotinamide mononucleotide treatment. β-nicotinamide mononucleotide treatment could effectively normalize the mitochondrial morphology and improve the function of mitochondria in senescent MSCs. [2]

METHODS: To study the effects on aging, β-nicotinamide mononucleotide (100-300 mg/kg) was administered in drinking water to normally aging wild-type C57BL/6N mice. The administration began at 5 months of age and continued for 12 months until the mice were 17 months old.
RESULTS: β-nicotinamide mononucleotide effectively attenuated age-related physiological decline in mice. β-nicotinamide mononucleotide did not have any significant toxic or deleterious effects, inhibited age-related weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and lipid levels, and improved insulin resistance. sensitivity and lipid levels, and improved eye function and other pathophysiology. [3]