NMN

Saka T, et al. Chemico-Biological Interactions, 2026, 431, 112012.

This study investigated the experimental application of β-nicotinamide mononucleotide (NMN) in preventing lipid peroxidation-derived aldehyde (HNE and ONE)-induced senescence in LX-2 hepatic stellate cells. LX-2 cells were pretreated with NMN prior to exposure to HNE to evaluate senescence-associated secretory phenotype (SASP) gene expression, SA-βGal activity, mitochondrial membrane potential, and lipid metabolism. NMN pretreatment significantly reduced Bax/Bcl2 ratio, restored mitochondrial membrane potential, and recovered intracellular NAD⁺ levels and SIRT1 activity. Western blotting and enzyme activity assays confirmed SIRT1 restoration, while lipid-metabolizing enzyme expression and intracellular lipid levels were assessed to evaluate metabolic recovery. These experimental results demonstrate that NMN effectively suppresses HSC senescence and lipid accumulation by restoring NAD⁺/SIRT1 signaling and mitochondrial function, highlighting its therapeutic potential in liver fibrosis research.

Cao Z, et al. mSphere, 2025, 10(8).

This study explored the application of β-nicotinamide mononucleotide (NMN) in a mouse model of hypervirulent Klebsiella pneumoniae bloodstream infection (hvKP BSI). NMN supplementation was administered alone or combined with antibiotic therapy, followed by macrophage depletion experiments to assess immune dependence. Bone marrow-derived macrophages were used to evaluate NF-κB pathway activation and inflammatory cytokine transcription (Il6, Il1b, Tnf, Cxcl2). NMN treatment significantly reduced NF-κB activation, suppressed inflammatory cytokine expression, and decreased neutrophil infiltration in liver tissue. Histological and biochemical analyses confirmed reduced liver abscess formation and improved survival. The experimental design demonstrates that NMN modulates macrophage-mediated inflammatory responses and enhances antibiotic efficacy, supporting its potential as an adjunct therapeutic strategy for hvKP-induced liver injury.

Tao H, et al. European Journal of Pharmacology, 2026, 1015, 178562.

This study evaluated β-nicotinamide mononucleotide (NMN) in a lipopolysaccharide-induced endotoxemia mouse model to investigate myocardial protection through Sirt5-mediated succinate dehydrogenase (SDH) regulation. NMN was administered intraperitoneally (500 mg/kg) for up to 28 days to monitor myocardial NAD⁺ levels and cardiac function. Cardiac injury markers (cTnI), ATP production, inflammatory cytokines, and oxidative stress were measured, while SDH activity and succinate metabolism were analyzed using biochemical assays. Immunoprecipitation and desuccinylation analysis confirmed enhanced Sirt5-SDH interaction and reduced SDH succinylation. Cardiomyocyte-specific Sirt5 knockdown abolished NMN's protective effects, validating the mechanism. These experimental findings demonstrate that NMN restores NAD⁺ levels, promotes Sirt5-dependent SDH desuccinylation, and corrects metabolic dysfunction, providing a mechanistic basis for NMN in cardiac protection during endotoxemia.

Li H, et al. Redox Biology, 2023, 63, 102745.

This study investigated β-nicotinamide mononucleotide (NMN) in a cecal ligation and puncture (CLP)-induced sepsis-associated encephalopathy mouse model and LPS-treated BV-2 microglial cells. NMN administration was used to restore hippocampal NAD⁺ levels and SIRT1 activity, followed by behavioral evaluation using Morris water maze and fear conditioning tests. Western blotting and biochemical assays measured PGC-1α expression, lysine acetylation, and NF-κB signaling activation. NMN significantly reduced hippocampal inflammation, oxidative stress, and apoptosis while improving cognitive performance. The use of SIRT1 inhibitor EX-527 and SIRT1 knockdown reversed NMN-mediated neuroprotection, confirming pathway specificity. These experimental results demonstrate that NMN alleviates sepsis-induced neuroinflammation and cognitive impairment through activation of the NAD⁺/SIRT1 signaling pathway.