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Fire Needle Acupuncture Regulates Wnt/ERK Multiple Pathways to Promote Neural Stem Cells to Differentiate into Neurons in Rats with Spinal Cord Injury
BACKGROUND & OBJECTIVE: NSCs therapy is considered one of the most potential methods for spinal cord injury (SCI). METHODS: We build the SCI model rats to investigate the therapeutic effect of fire needle acupuncture in improving the locomotor function of SCI rats and its possible mechanism. BBB...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bentham Science Publishers
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6806613/ https://www.ncbi.nlm.nih.gov/pubmed/30714534 http://dx.doi.org/10.2174/1871527318666190204111701 |
Sumario: | BACKGROUND & OBJECTIVE: NSCs therapy is considered one of the most potential methods for spinal cord injury (SCI). METHODS: We build the SCI model rats to investigate the therapeutic effect of fire needle acupuncture in improving the locomotor function of SCI rats and its possible mechanism. BBB scale was used for the motor ability of rats. The expression of Nestin, NSE, Gal-C, and GFAP was detected by immunohistochemistry. Wnt, GSK3β, β-catenin, ERK1/2, CyclinD1, and ngn1 were detected by western blot and PCR. The BBB score of both model group (1.20±0.94, 3.12±0.67, 5.34±1.57, 7.12±1.49) and fire needle group (1.70±0.58, 4.50±1.63, 7.53±2.41, 9.24±0.63) gradually increased after SCI. Furthermore, at d10 and d14, the fire needle group showed a significantly high score compared with that in model group at the same time (P<0.05). Fire needle increased Nestin, NSE, and Gal-C expression inhibited GFAP expression after SCI. Also, fire needle could up-regulate Wnt3a, GSK3β, β-catenin, and ngn1, and down-regulate ERK1/2, cyclinD1 gene and protein expression. CONCLUSION: In conclusion, fire needle could improve lower limb locomotor function of SCI rats. Also, fire needles could promote endogenous NSCs proliferation differentiating into neurons, and the mechanism might be mediated by promoting the activation of Wnt/β-catenin and inhibiting the overexpression of ERK. |
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