ArticleFrontiers in neurology
Atractylodin alleviates neuroinflammation and protects neurological function after ischemic stroke in association with reduced NLRP3 inflammasome activation.
Article in Frontiers in neurology. 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
Background: NOD-like receptor protein 3 (NLRP3) inflammasome-driven neuroinflammation contributes to ischemic stroke injury. Atractylodin (ART) shows anti-inflammatory activity, but its neuroprotective potential and mechanistic links to NLRP3 signaling after cerebral ischemia-reperfusion (I/R) injury remain to be defined. Materials and methods: BV2 microglia were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R), and rats underwent middle cerebral artery occlusion (MCAO) followed by reperfusion. ART was administered after reperfusion Results: In OGD/R-stimulated BV2 microglia, ART suppressed NLRP3 inflammasome activation and reduced GSDMD cleavage, accompanied by decreased IL-1β and IL-18 production. In the MCAO model, ART significantly improved neurological outcomes and reduced infarct volume and neuronal apoptosis. These protective effects were linked to a reduction in the expression of NLRP3 pathway components (NLRP3, ASC, and caspase-1) and GSDMD-N. Additionally, there was a shift in microglial responses toward an anti-inflammatory (M2-like) profile, which led to a decrease in pro-inflammatory markers. Conclusion: ART confers neuroprotection in experimental ischemic stroke by inhibiting NLRP3 inflammasome-associated pyroptosis and modulating microglial inflammatory polarization, supporting its potential as a therapeutic candidate for ischemic stroke.
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