Neuroprotective effects of salidroside against cerebral ischemia-reperfusion injury involve downregulation of total NAMPT and suppression of microglial inflammation

Objective: This study investigated the protective effect of Salidroside (SAL) against cerebral ischemia-reperfusion (I/R) injury and its role in regulating nicotinamide phosphoribosyltransferase (NAMPT)-mediated neuroinflammation and damage. Methods: , primary microglia were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) and divided into control (Ctrl), OGD-NS, OGD+eNAMPT (20 ng/mL), and OGD+eNAMPT+SAL (6 μg/mL) groups. Cytotoxicity (LDH), viability (MTT), and IL-1β/TNF-α secretion (ELISA) were measured. Results: < 0.001). Conclusion: This study provides experimental evidence that the neuroprotective effects of SAL against cerebral I/R injury are associated with downregulation of pathologically elevated NAMPT expression (likely reflecting a reduction in pro-inflammatory eNAMPT), restoration of cerebral NAD+ homeostasis (potentially preserving iNAMPT function), and suppression of microglia-mediated neuroinflammation, suggesting that eNAMPT may serve as a potential effector molecule of SAL.