ArticleJournal of inflammation research2025
Electroacupuncture Improves Learning and Memory Impairment in Rats with Cerebral Ischemia/Reperfusion Injury by Promoting Microglia/Macrophage M2 Polarization Through Nrf2/HO-1 Pathway.
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 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.Molecular neurobiology · 2026Review
- Electroacupuncture Modulates Multiple Pathways for Neuroprotection and Neurorepair in Ischemic Stroke.CNS neuroscience & therapeutics · 2026Review
- Novel insights of acupuncture in ischemic stroke: orchestrating neuro-endocrine-immune network.Frontiers in immunology · 2026Review
- From arthritis to central sensitization: targeting the neuro-immune axis via microglial modulation in acupuncture treatment for Juvenile Idiopathic Arthritis-associated pain.Frontiers in immunology · 2025Review
- Iron homeostasis and macrophage polarization in pulmonary fibrosis: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
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Authors and funding
9 authors.
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Abstract
Objective: While electroacupuncture (EA) has shown effectiveness in treating learning and memory deficits associated with ischemic stroke (IS), the specific mechanisms involved remain unclear. The goal of this study was to investigate whether EA improves learning and memory deficits in MCAO rats by regulating microglia/macrophage polarization through the nuclear factor red lineage 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Methods: Sprague-Dawley rats were subjected to MCAO modeling and treated with EA 24 hours post-MCAO for a period of two weeks. To investigate the involvement of Nrf2/HO-1 in the effects of EA, tin protoporphyrin (SnPPIX), an inhibitor of HO-1, was injected into the left ventricle of rats before initiating EA treatment. Neurological function in MCAO rats was evaluated using a neurological deficit score. The effects of EA on learning and memory deficits were assessed using the Morris water maze (MWM) and open field test (OFT). Hematoxylin-Eosin (HE) staining was used to observe hippocampal structural morphology, and 2,3,5-Triphenyltetrazolium Chloride (TTC) staining was used to assess the infarct volume. Protein expression levels of the Nrf2/HO-1 signaling pathway and microglial/macrophage polarization were determined using ELISA, immunofluorescence double-labeling, Western blotting (WB), and real-time quantitative polymerase chain reaction PCR (qRT-PCR). Results: EA significantly enhanced learning and memory function in rats by upregulating NRF2/HO-1 expression and promoting M2 polarization of microglia/macrophages. However, administration of SnPPIX, an HO-1 inhibitor, counteracted the beneficial effects of EA on memory improvement in MCAO rats, while also worsening cerebral infarct volume and inflammatory response. Conclusion: EA effectively improved learning and memory impairments in MCAO rats by activating the Nrf2/HO-1 signaling pathway, leading to the promotion of M2 polarization in microglia/macrophages.
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