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Nicotinamide Riboside Blocks LPS-Induced Microglial Inflammation: Preclinical Findings
Synopsis
In LPS-stimulated BV2 microglia, nicotinamide riboside (NR) restored mitochondrial function and reduced inflammation by activating the AMPK–SIRT3 signaling axis. NR shifted microglia from a pro-inflammatory M1 state toward an anti-inflammatory M2 state, lowered inflammatory and glycolytic gene expression, and upregulated genes involved in mitochondrial biogenesis. Blocking SIRT3 reduced AMPK phosphorylation and worsened inflammation, while activating SIRT3 or adding NR reversed these effects. Likewise, inhibiting AMPK decreased SIRT3 expression and mitochondrial biogenesis, whereas AMPK activation countered LPS-induced dysfunction. These findings highlight AMPK and SIRT3 as essential regulators of microglial metabolism and inflammation and show that NR exerts its neuroprotective, anti-inflammatory effects by engaging the AMPK–SIRT3 pathway, supporting its potential use in neurodegenerative disease management.
Journal
Food Bioscience