ArticleJournal of inflammation research2025
Electroacupuncture at ST36 Treatment Suppresses the Microglial Pyroptosis Through Activating α7nAChR in a Rat Model of Asphyxial Cardiac Arrest.
Article in Journal of inflammation research, 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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Who cites it
2 citing papers in PubMed.
- Nasal-to-Brain ROS-Responsive Diselenide-Bridged Graphene Nanogel for Targeted Ischemic Stroke Therapy via Microglial Modulation.ACS omega · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
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10 authors.
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Abstract
Background: Neuroinflammation is a critical element to cardiac arrest (CA)-induced global cerebral ischemia injury. Electroacupuncture (EA) treatment has demonstrated therapeutic potentials in both animal and clinical studies for the cerebral ischemic treatment. Nevertheless, the neuroprotective effect of electroacupuncture at ST36 (EA-ST36) in CA-induced global cerebral ischemia injury and the underlying mechanisms remains unclear. Methods: Using a rat model of Asphyxial Cardiac Arrest, the neuroprotective effects of EA-ST36 were evaluated. Single cell RNA-seq analyses were performed to assess the genetic expression of pyroptosis in different cell types of brain. Cognitive performance was tested through the Morris water maze, while neuronal survival, microglial pyroptosis, and neuroinflammation were analyzed by immunofluorescence, flow cytometry, ELISA, and histopathological staining. An oxygen-glucose deprivation/reoxygenation (OGD/R) model of primary microglia was established to confirm the role of α7nAChR in inhibiting pyroptosis. Results: Single-cell RNA sequencing of rat brain and immunofluorescent co-localization showed that pyroptosis is principally occurred in microglia rather than neurons, astrocytes, oligodendrocytes, or endothelial cells in CA/CPR rats. EA-ST36 treatment significantly improved spatial learning and memory in CA/CPR rats, reduced neuronal loss, and attenuated neuroinflammation. These neuroprotective effects were associated with suppressed microglial pyroptosis and decreased IL-1β and IL-18 levels. Remarkably, these neuroprotective effects were abolished by α7nAChR inhibitors. In vitro, α7nAChR activation suppressed OGD/R-induced microglial pyroptosis by inhibiting expression of NLRP3, cleaved caspase-1, and N-GSDMD, and decreased IL-1β and IL-18 levels and alleviated the neurotoxic effects of pyroptotic microglia. Conclusion: Our study revealed that EA-ST36 exerted neuroprotective effects with a potent anti-neuroinflammatory potential by suppressing microglial pyroptosis in a rat CA/CPR model, and these anti-neuroinflammatory properties are α7nAChR-dependent.
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