Nicotinamide Mononucleotide Is Associated with Attenuation of OGD/R-Induced Pro-Inflammatory Programs in Microglia: Transcriptomic Evidence Converging on the NLRP3 Inflammasome and Lipid-Droplet-Related Molecular Signatures

Background

Hypoxic-ischemic brain injury triggers persistent microglial hyperactivation, which drives progressive secondary neuroinflammation and subsequent neurological deficits. Nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD+) precursor, confers neuroprotective effects in neonatal hypoxic-ischemic injury models. Nevertheless, the molecular landscape linking NMN treatment to metabolic and inflammatory reprogramming in microglia remains incompletely characterized.