Systemic nicotinamide mononucleotide administration to mitigate post-cardiac arrest brain injury in mice.

ABSTRACT: Post-cardiac arrest brain injury (PCABI) is the leading cause of death and disability following cardiac arrest (CA). Nicotinamide adenine dinucleotide (NAD+) depletion after CA contributes to neuronal injury, while nicotinamide mononucleotide (NMN) replenishes NAD+ and may provide neuroprotection via sirtuin activation. This study aimed to investigate the effects of systemic NMN administration on neurological function, survival, and sirtuin-3 (SIRT3) levels in the brain post-CA. In adult male mice (C57BL/6NCrSlc, 10-15 weeks old), 10-min CA was induced by intravenous potassium chloride injection followed by cardiopulmonary resuscitation. NMN (60 mg/kg body weight) or normal saline (control) was randomly administered by intraperitoneal injection immediately after the return of spontaneous c

SUBMITTER: Kaito D 

PROVIDER: S-EPMC12539731 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature