ArticleCNS neuroscience & therapeutics2026
Scutellarin Alleviates Neuronal Apoptosis After Ischemia and Hypoxia via the HIF-1α-CX3CR1 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
backgroundStroke is a significant health threat characterized by high incidence, mortality, disability, recurrence, and complications. Over 70% of strokes are ischemic in nature. Reducing neuronal apoptosis following ischemic-hypoxic injury is crucial for effective treatment. This study investigates the direct neuroprotective effects of scutellarin after ischemia-hypoxia, clarifies the relationship between upregulated CX3CR1 expression and neuronal apoptosis, and elucidates the mechanism by which scutellarin regulates apoptosis through the HIF-1α-CX3CR1 axis. This research provides a robust theoretical foundation for the clinical application of scutellarin in the management of ischemic stroke.
methodsA mouse model of transient middle cerebral artery occlusion (tMCAO) was established in vivo, and an oxygen-glucose deprivation/reoxygenation (OGD/R) model was constructed by culturing primary neuronal cells in vitro. The direct protective effects of scutellarin on neurons following ischemia and hypoxia were observed, along with its impact on neurological function and cerebral infarct volume. Changes in the expression of neuronal CX3CR1 and its effects on apoptosis after ischemia and hypoxia were determined using immunofluorescence, Western blotting, and CX3CR1 transgenic mice. Finally, quantitative PCR (Q-PCR), immunofluorescence, and Western blotting were employed to investigate whether scutellarin modulates NF-κB via the HIF-1α-CX3CR1 axis and the JAK1-STAT1 pathway, thereby influencing neuronal apoptosis.
resultsIn vitro and in vivo experiments have demonstrated that scutellarin reduces neuronal apoptosis, thereby decreasing the infarct area and alleviating neurological deficits in MCAO mouse models. Following ischemia and hypoxia, the expression of CX3CR1 in neurons is upregulated, which mediates neuronal apoptosis. Scutellarin downregulates the expression of CX3CR1 by modulating HIF-1α. Additionally, CX3CR1 can regulate neuronal apoptosis after ischemia through the NF-κB/P65 and JAK1-STAT1 signaling pathways.
conclusionsOur experimental results confirm that scutellarin regulates neuronal apoptosis following ischemia and hypoxia through the HIF-1α-CX3CR1 axis. These findings provide additional theoretical evidence for the clinical application of scutellarin and suggest potential therapeutic targets for the treatment of ischemic stroke.
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