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Electroacupuncture alleviates central post-stroke pain in rats by modulating miR-21-5p/TGF-β/Smads pathway
Guihua Tian1, Yang Wu2, Zhihao Shang3
1Beijing Friendship Hospital, Capital Medical University, No. 95, Yong'an Road, Xicheng District, Beijing, 100032, China. rosetgh@163.com.
The Journal of Headache and Pain
|December 26, 2025
Summary
Electroacupuncture (EA) alleviates central post-stroke pain by downregulating miR-21 and inhibiting the TGF-β/Smads pathway. This study reveals EA
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Central post-stroke pain (CPSP) is a challenging condition with limited treatment options.
- MicroRNA-21 (miR-21) and the TGF-β/Smads pathway are implicated in pain.
- The role of miR-21/TGF-β/Smads in electroacupuncture (EA) for CPSP is unclear.
Purpose of the Study:
- To investigate if EA's analgesic effect in CPSP is mediated by the miR-21/TGF-β/Smads pathway.
- To explore the molecular mechanisms of EA in CPSP.
Main Methods:
- CPSP was induced in rats via stereotactic collagenase-IV injection.
- miR-21-5p and Smad7 levels were manipulated using adenoviral vectors.
- Pain thresholds, neuronal damage, glial activation, and inflammatory markers were assessed.
- A dual-luciferase reporter assay confirmed direct interaction between miR-21-5p and Smad7.
Main Results:
- EA significantly reduced CPSP and neuroinflammation markers.
- EA downregulated miR-21-5p and upregulated Smad7, decreasing TGF-β1, p-Smad2, and p-Smad3.
- Inhibition of miR-21-5p mimicked EA's analgesic effect; its overexpression or Smad7 inhibition reversed EA's benefits.
Conclusions:
- EA analgesia in CPSP involves downregulating miR-21-5p.
- This action inhibits neuroinflammation via the Smad7/TGF-β/Smads pathway.
- Provides novel molecular insights into EA's mechanism for pain relief.

