ArticleFrontiers in aging neuroscience2025
Ginsenoside Rb1 attenuates neuroflammation via activating Wnt/β-catenin signaling pathway to exert neuroprotective effect on cerebral ischemic-reperfusion injury.
Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Multi-omics analysis of untargeted metabolomics and gut microbiota study on the mechanism of Astragalus-Safflower to coordinate the regulation of energy metabolism pathways and gut microbiota remodeling to improve ischemic stroke.Metabolic brain disease · 2026Article
- Use of Laser Speckle Contrast Imaging for Distribution of Animals by Severity of Brain Tissue Damage in a Neonatal Hypoxia-Ischemia Model in Mice.Brain sciences · 2026Article
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6 authors.
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Abstract
Purpose: To explore the molecular mechanism of G-Rb1 regulating microglia polarization through Wnt/β-catenin signaling pathway to alleviate cerebral ischemia-reperfusion injury in mice. Methods: C57BL/6J mouse middle cerebral artery occlusion/reperfusion (MCAO/R) model and microglia (BV2) oxygen-glucose deprivation/reoxygenation (ODG/R) model were used. The neuroprotective effect of G-Rb1 Results: Compared with the Sham group, the symptoms of neurological impairment, cerebral blood perfusion, cerebral infarction volume and inflammatory reaction were increased in the IRI group. Compared with the IRI group, G-Rb1 group showed less symptoms of neurological impairment, increased cerebral blood perfusion, decreased cerebral infarction volume, increased proportion of M2-type microglia, increased release of anti-inflammatory factors, reduced inflammatory response, and up-regulated β-catenin expression while down-regulated GSK-3β expression. It was demonstrated that G-Rb1 activates the Wnt/β-catenin signaling pathway after CIRI. Compared with G-Rb1 group, G-Rb1 + XAV939 group had more neurological impairment, increased cerebral infarction volume, increased M1 microglia proportion, and increased neuroinflammation. Meanwhile, β-catenin expression decreased while GSK-3β expression increased. The results of
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