ArticleIBRO neuroscience reports2025
Electroacupuncture mitigates cognitive impairments in chronic hypoxia-induced mice by modulating neuroinflammation.
Article in IBRO neuroscience reports, 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.
- Electroacupuncture Ameliorates Learning and Memory Deficits in Vascular Cognitive Impairment Rats Through Activation of the Supramammillary Nucleus-Dentate Gyrus Circuit.CNS neuroscience & therapeutics · 2026Article
- Efficient combined use of electroacupuncture with ordered collagen scaffolds enhances the therapeutic efficacy of human spinal cord-derived neural progenitor cells therapy in spinal cord injury rats.Science China. Life sciences · 2026Article
- Review
- Electroacupuncture Prevents Against AD-Like Phenotypes in APP/PS1 Mice: Investigation of the Mechanisms From Cerebral Microangiopathy.CNS neuroscience & therapeutics · 2025Article
- Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway.Neurochemical research · 2025Article
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10 authors.
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Abstract
This study investigates the therapeutic effects and mechanisms of electroacupuncture (EA) on cognitive impairment induced by chronic hypoxia (CH) in mice. Chronic hypoxia was simulated by exposing mice to a 10 % oxygen environment for 8 hours daily over 3 months. The cognitive functions of the mice were assessed through behavioral tests, including the open field test (OFT), Y-maze, and Morris water maze (MWM). Results showed that CH induced significant anxiety-like behaviors and memory impairments in mice. EA treatment, targeting the Baihui (GV20), Shenting (GV24), and Zusanli (ST36) acupoints, significantly ameliorated these behavioral deficits. Histological analyses using HE staining, Nissl staining, and TUNEL assays demonstrated that EA reduced neuronal damage, apoptosis, and myelin loss in the cerebral cortex and hippocampus. Additionally, EA treatment significantly lowered the expression of the pro-inflammatory cytokine TNF-α in brain tissues, suggesting its anti-inflammatory effects. Immunofluorescence and Western blot analyses revealed that EA inhibited the overactivation of microglia and astrocytes in the CH model. Specifically, EA suppressed the expression of Iba1 and GFAP, markers of microglial and astrocytic activation, respectively. Furthermore, EA promoted the polarization of microglia towards the M2 anti-inflammatory phenotype by downregulating iNOS and upregulating Arg1. Similarly, EA reduced the expression of C3, a marker of A1 astrocytes, thereby preventing astrocytic polarization towards the pro-inflammatory state. Organotypic brain slice cultures subjected to oxygen-glucose deprivation (OGD) confirmed that electrical stimulation, akin to EA, inhibited the activation of microglia and astrocytes under hypoxic conditions. In conclusion, EA improves cognitive function in CH-induced mice by reducing neuroinflammation, inhibiting glial cell overactivation, and promoting anti-inflammatory phenotypes. These findings highlight EA's potential as a therapeutic intervention for cognitive impairments related to chronic hypoxia.
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