ArticlePloS one2025
Systemic nicotinamide mononucleotide administration to mitigate post-cardiac arrest brain injury in mice.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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 circulation (ROSC) and 24 and 48 h post-CA. Brain NAD+ and adenosine triphosphate (ATP) levels, neurological function score (NFS), survival, histological neuronal injury, and brain gene expression and protein levels were measured. Brain NAD+ levels decreased at 2 h post-ROSC and NMN significantly increased brain NAD+ and ATP levels. At 48 h post-CA, surviving mice in the NMN group exhibited significantly higher NFS (control: 8 [IQR: 4-12] vs. NMN: 12 [IQR: 9-12], p = 0.03) and less severe hippocampal neuronal injury compared with controls. Moreover, the NMN group showed significantly higher 7-day survival rate (control: 22.2% [4/18] vs. NMN: 61.1% [11/18], p = 0.03) and brain SIRT3 levels (control: 17.7 ± 3.6 vs. NMN: 34.5 ± 4.4 pg/mg protein, p = 0.01). In conclusion, systemic NMN administration after ROSC attenuates PCABI. The increased brain ATP levels and SIRT3 upregulation may suggest the usefulness of NMN for improving mitochondrial function and contributing to neuroprotection. NAD+ supplementation with NMN is a promising therapeutic approach against PCABI.
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