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Mol Med Rep. 2017 Aug;16(2):2185-2190. doi: 10.3892/mmr.2017.6801. Epub 2017 Jun 19.

Recovery of spinal cord injury following electroacupuncture in rats through enhancement of Wnt/β-catenin signaling.

Author information

1
Department of Acupuncture, Tuina and Traumatology, The Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, P.R. China.

Abstract

Electroacupuncture (EA) has been demonstrated to promote the functional recovery of neurons following spinal cord injury (SCI); however, the mechanisms underlying its effects have yet to be elucidated. The Wnt/β-catenin signaling pathway has been implicated in the regulation of the balance between growth, proliferation and differentiation of neural precursor cells. The present study aimed to investigate the effects of EA therapy on Wnt/β‑catenin‑regulated gene expression and neuronal recovery in rats with SCI. The Allen method was used to establish SCI in rats, and alterations in Wnt1 and Nestin mRNA and protein expression levels in response to SCI were determined on days 1, 3, 7 and 14 post‑injury using reverse transcription‑quantitative polymerase chain reaction and western blot analysis. To evaluate the effects of EA treatment on SCI, the following four treatment groups were employed: SCI, SCI + EA, SCI + lithium chloride (LiCl) and SCI + LiCl + EA. The protein expression levels of Wnt1, Nestin and nuclear β‑catenin were evaluated on day 3 post‑treatment, and neuronal nuclear antigen (NeuN) protein expression levels were evaluated on day 21 post‑treatment using western blot analysis. The Basso, Beattie and Bresnahan scoring method was used to evaluate spinal cord recovery on day 28 post‑treatment across the four treatment groups. EA therapy at the Dazhui and Mingmen acupuncture points significantly increased the expression levels of Wnt1, Nestin, β‑catenin and NeuN, thus suggesting that EA therapy may promote spinal cord recovery following injury. The underlying mechanism was demonstrated to involve enhanced Wnt/β‑catenin signaling, which may promote the proliferation and differentiation of neural stem cells. However, further studies are required to elucidate the detailed effects and underlying molecular mechanisms of EA therapy on SCI.

PMID:
28627669
DOI:
10.3892/mmr.2017.6801
[Indexed for MEDLINE]

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