ArticleNeurochemical research2025
Electroacupuncture Ameliorates Neuroinflammatory Injury in CPSP Rats by Inhibiting the LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway.
Article in Neurochemical 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.
- The Molecular Mechanism of LncRNA LUCAT1 Regulating HSPB8 Expression via miR-337-3p in Modulating Neurological Damage After Cerebral Infarction.Neurochemical research · 2026Article
- The LINC00968/miR-194-5p Axis Exacerbates Neurological Dysfunction After Intracerebral Hemorrhage by Regulating Oxidative Stress and Neuroinflammation.Neurochemical research · 2025Article
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12 authors.
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Abstract
Electroacupuncture (EA) therapy has been shown to significantly alleviate central poststroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explored the role of EA in ameliorating central nervous system inflammation in CPSP rats.The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus (VPL). The treatment group was treated with 15 Hz and 2 mA continuous wave EA every other day for a total of 8 sessions. The lncRNA MEG3 (MEG3) was knocked down or overexpressed by adeno-associated virus delivery in vivo in the rat brain. Pain thresholds were measured to assess the hypersensitivity of the rats to pain. Immunofluorescence, Nissl staining and enzyme-linked immunosorbent assay (ELISA) were used to assess the levels of MEG3 and glial fibrillary acidic protein (GFAP) in VPL brain tissue, neuronal injury, and the levels of substance P (SP), TNF-α, IL-1β and IL-6 in VPL brain tissue and serum, respectively. The levels of MEG3, Wnt3a, β-catenin and GFAP in VPL brain tissue were assessed by qRT‒PCR or Western blotting. EA inhibits the expression of MEG3 and neuroinflammatory injury in the VPL brain tissue of CPSP rats, ameliorating hyperalgesia symptoms in CPSP rats. The overexpression of MEG3 weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the VPL region of the brain, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of MEG3 in the VPL brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. EA could alleviate neuroinflammation and reduce pain in CPSP rats by suppressing the expression of MEG3. EA could regulate the Wnt/β-catenin signaling pathway via MEG3.
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