ArticleCNS neuroscience & therapeutics2026
Polydatin Inhibits Neuroinflammation in Cerebral Ischemia-Reperfusion Injury Through Suppressing the CXCL3/CXCR2 Axis.
Article in CNS neuroscience & therapeutics, 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
aimThe aim of this study is to investigate the precise mechanisms by which Polydatin (PD) ameliorates cerebral ischemia-reperfusion injury (CIRI).
methodsWe first established a rat model of CIRI to evaluate PD's therapeutic effects. Transcriptomic analysis was used to explore PD's impact on gene expression in ischemic brain tissue of CIRI rats. OGD/R-induced microglial activation experiments validated that PD inhibits microglial activation by targeting the CXCL3/CXCR2 axis.
resultsPD intervention improved neurological function scores of CIRI rats, reduced infarct area, alleviated pathological damage, and preserved Nissl bodies in brain tissue. It also modulated oxidative stress levels. Transcriptomic analysis showed enrichment of the Cytokine-cytokine receptor interaction pathway and several inflammatory pathways after PD intervention, with downregulation of CXCL3 and CXCR2. PD decreased pro-inflammatory cytokine levels and CXCL3/CXCR2 protein expression in ischemic brain tissue of CIRI rats, and reduced positive expression areas of IBA1
conclusionOur findings suggest that PD can inhibit microglial migration and activation by acting on the CXCL3/CXCR2 axis, thereby alleviating the inflammatory response in CIRI.
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