ArticleThe journal of headache and pain2025
Electroacupuncture alleviates central post-stroke pain in rats by modulating miR-21-5p/TGF-β/Smads pathway.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Electroacupuncture for temporomandibular disorder-related pain: clinical evidence, mechanisms, and safety-a narrative review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundCentral post-stroke pain (CPSP) poses a persistent challenge with limited responses to current pharmacological interventions. Recent evidence implicates miR-21 and its downstream TGF-β/Smads signaling pathway in pain pathophysiology. This study investigates whether the analgesic effect of electroacupuncture (EA) is related to miR-21/TGF-β/Smads signaling pathway in CPSP.
methodsCPSP was induced in rats by collagenase-IV injection into the right thalamic ventral posterolateral nucleus to produce a focal hemorrhagic stroke lesion. miR-21-5p and Smad7 expressions were manipulated by adenoviral transfection. Pain thresholds were assessed during 15 days after CPSP induction, followed by brain tissue analysis using nissl staining, immunofluorescence, immunohistochemistry, and molecular assays. A dual-luciferase reporter assay was employed to verify the direct binding interaction between miR-21-5p and Smad7.
resultsThe results showed EA significantly alleviated CPSP, and meanwhile, downregulated miR-21-5p, upregulated Smad7, and reduced TGF-β1, p-Smad2, and p-Smad3 expressions, glial hyperactivation and inflammatory factors (IL-1β, IL-6, TNF-α) in CPSP rats. In addition, miR-21-5p inhibition resulted in analgesic effect, while miR-21-5p overexpression or Smad7 inhibition counteracted the effect of EA.
conclusionsThese results indicate that the mechanisms underlying EA-induced analgesia involve downregulating miR-21-5p, consequently inhibiting neuroinflammation by regulating Smad7/TGF-β/Smads signaling pathway, providing a novel insight for probing the molecular mechanism of analgesic effect of EA.
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