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Electroacupuncture Improves the Motor Function in Rats with Spinal Cord Injury by Regulating UCN2-Mediated cAMP-PKA
Yinjie Hu1, Xiaolong Tang2, Siwen Li3
1School of Acupuncture-Moxibustion and Tuina, Shanghai University of Traditional Chinese Medicine, Shanghai, 200120, China.
Cellular and Molecular Neurobiology
|March 26, 2025
Summary
Electroacupuncture (EA) improves hind-limb function after spinal cord injury (SCI) by modulating urocortin 2 (UCN2) and activating the cAMP-PKA pathway. This treatment reduces glial scarring and neuronal apoptosis, promoting recovery.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Traditional Chinese Medicine
Background:
- Spinal cord injury (SCI) leads to significant mortality and disability, causing severe neurological deficits.
- Urocortin 2 (UCN2) is implicated in spinal cord motor function regulation.
- The precise role of electroacupuncture (EA) in modulating UCN2 post-SCI and its mechanisms remain largely unknown.
Purpose of the Study:
- To investigate the therapeutic effects of EA on SCI in a rat model.
- To elucidate the role of UCN2 and its downstream signaling pathways in EA's recovery mechanisms.
- To assess EA's impact on cellular changes and locomotor function at various time points post-injury.
Main Methods:
- Established a complete spinal cord transection model in Sprague-Dawley rats.
- Administered EA to T9 and T11 Jiaji points.
- Conducted behavioral analyses, histological assessments, RNA sequencing, and molecular validation (qPCR, Western blotting, immunohistochemistry).
Main Results:
- EA significantly improved locomotor function at 7, 14, and 28 days post-injury (d.p.i.).
- EA modulated glial scar formation, reduced astrocyte proliferation, and suppressed neuronal apoptosis at 3 d.p.i.
- EA altered microglial numbers, increased neurofilament and myelin basic protein expression at later time points, and modulated UCN2 expression and cAMP-PKA signaling.
Conclusions:
- EA effectively promotes functional recovery after SCI by modulating UCN2 expression and activating the cAMP-PKA signaling pathway.
- EA influences glial responses, reduces neuronal apoptosis, and enhances axonal regeneration and remyelination.
- EA represents a promising therapeutic strategy for managing spinal cord injuries.

