Administration of β-Nicotinamide Mononucleotide Attenuates Myocardial Dysfunction in Tail-Suspended Mice

Abstract

Microgravity conditions cause myocardial atrophy and dysfunction with limited therapeutics. Accumulating evidence demonstrates that the deficiency of nicotinamide adenine dinucleotide (NAD+) contributes to myocardial dysfunction under microgravity, making NAD+boosting an appealing therapeutic approach. In this study, we sought to investigate whether β-nicotinamide mononucleotide (NMN), a precursor of NAD+, preserved cardiomyocytes size and myocardial function during microgravity. Simulated microgravity was induced by tail-suspension in C57BL/6 mice for 28 days. NMN (100 mg/kg body weight) was given every other day after the onset of tail-suspension. Tail-suspension reduced the NAD+content in hearts and decreased the heart weight and cardiomyocytes size, and cardiac function. Administration of NMN attenuates myocardial atrophy and preserves myocardial function in tail-suspended mice. These cardioprotective effects of NAD+repletion were associated with the reduction of oxidative stress and improvement of autophagic flux. These findings indicate that NMN may hold great potential as a therapeutic approach for myocardial abnormalities under microgravity conditions.