ArticleFrontiers in pharmacology2026
Neuroprotective effects of salidroside against cerebral ischemia-reperfusion injury involve downregulation of total NAMPT and suppression of microglial inflammation.
Article in Frontiers in pharmacology, 2026. 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
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: Results: Compared to Sham, the I/R group showed worsened neurological deficits, larger infarct volumes, elevated total NAMPT, TNF-α, and IL-1β levels ( 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.
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