Related Experiment Video
Updated: Apr 14, 2026
Author Spotlight: Establishing a Reliable Distal MCA Occlusion Model in Mice for Stroke Research
Published on: December 15, 2023
Atractylodin alleviates neuroinflammation and protects neurological function after ischemic stroke in association
Qingyao Ouyang1, Yiying Yang2, Hoi Leong Lee3
1College of Basic Medical Sciences, China Three Gorges University, Yichang, Hubei, China.
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 in vivo (10 or 30 mg/kg, once daily for 3 days) and during reoxygenation in vitro. Neurobehavioral outcomes and infarct volume were assessed in MCAO rats, along with measurements of neuronal apoptosis. NLRP3 inflammasome activation, gasdermin D (GSDMD)-dependent pyroptosis, pro-inflammatory cytokines, and microglial polarization markers were evaluated using immunoblotting, immunofluorescence, RT-qPCR, and enzyme-linked immunosorbent assay (ELISA).
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.
