ArticleNeurochemical research2025
Electroacupuncture Alleviates Cerebral Ischemia-Reperfusion Injury by Downregulating IL-17 A and Inhibiting Neurotoxic Astrocyte Activation.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Acupuncture for Poststroke Dysphagia: An NTS-Centered Hypothesis-Generating Framework Linking the Brainstem Swallowing Network, Neuroimmune Regulation, and Vagal Anti-Inflammatory Signaling.Brain and behavior · 2026Review
- Article
- The IL-17A modulating astrocytic activity was associated with the electroacupuncture-mediated improvement of sensorimotor ability after stroke.Chinese medicine · 2026Article
- Electroacupuncture Promotes Synaptic Recovery After Cerebral Ischemia-Reperfusion by Activating SIRT1 to Inhibit the NF-κB Pathway and Regulate Astrocyte Phenotypic Transformation.Neurochemical research · 2026Article
- Advances in the mechanisms of electroacupuncture in the treatment of cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
Cerebral ischemia-reperfusion injury (CIRI) represents a critical pathological mechanism underlying ischemic stroke, yet effective therapeutic interventions remain limited. Neurotoxic astrocytes, activated by inflammatory mediators such as interleukin-17 A (IL-17 A), exacerbate neuronal damage. Although electroacupuncture (EA) has demonstrated neuroprotective properties, its influence on IL-17 A signaling and subsequent astrocyte-mediated neurotoxicity in CIRI remains unclear. This study aims to investigate whether EA mitigates CIRI by downregulating IL-17 A to suppress the activation of neurotoxic astrocyte. A mouse model of middle cerebral artery occlusion and reperfusion (MCAO/R) was established employing the Zea-Longa modified ligation method. EA was applied to the Baihui (GV20) and Fengfu (GV16) acupoints. Neurological and behavioral evaluations were performed using the Modified Neurological Severity Score (mNSS), foot fault test, and balance beam test. Cerebral infarction volume was quantified via TTC staining, and neuronal ultrastructure was examined by transmission electron microscopy. Laser speckle imaging was employed to monitor cerebral blood flow before and after modeling and EA treatment. Western blotting was used to analyze protein expression levels of IL-17 A, IL-17RA, NF-κB p65, Bax, Bcl-2, and cleaved-Caspase-3/Caspase-3. Co-localization of IL-17 A with GFAP and C3, as well as IL-17RA with GFAP, was assessed via immunofluorescence staining. qPCR was performed to quantify IL-17 A mRNA levels, while TUNEL staining assessed neuronal apoptosis. ELISA was used to determine the concentrations of IL-17 A, TNF-α, and IL-1β in brain tissue. EA significantly improved neurological function, reduced cerebral infarct size, and alleviated neuronal apoptosis. Compared to the MCAO/R group, EA markedly downregulated IL-17 A expression and its related signaling proteins, inhibited neurotoxic astrocyte activation (C3⁺/GFAP⁺), and suppressed the release of proinflammatory cytokines. Notably, administration of recombinant IL-17 A reversed the neuroprotective effects of EA. These findings suggest that EA mitigates ischemic brain injury by inhibiting IL-17 A-mediated neurotoxic astrocyte activation and neuroinflammation, highlighting its potential as a therapeutic strategy for CIRI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.