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Spinal cord injury is one of the serious central nervous system injuries and the incidence of spinal cord injury continues to increase. Previous studies have indicated that electroacupuncture is beneficial for promoting recovery after spinal cord injury. In the present study, we attempted to evaluate how electroacupuncture can promote the neural repair in spinal cord injury model rats by observing changes in the Notch signaling pathway.
Experimental rats were randomly divided into four groups. Each group had its own intervention period: 1 day, 7 days, 14 days, and 28 days, and five randomized subgroups: blank control (B) group, blank electroacupuncture (BE) group, sham operation (S) group, model control (M) group and electroacupuncture group. Animals in the electroacupuncture group and the BE group were treated with electroacupuncture at Dazhui (GV14) and Mingmen (GV4) acupoints for 20 min. After the intervention period, the Basso-Beattie-Bresnahan (BBB) score was used to evaluate the neurological function.
We found that BBB score increased in electroacupuncture-treated groups. Hematoxylin and eosin staining was used to observe pathological changes in the injured spinal cord and the results showed that electroacupuncture therapy could promote the repair of injured spinal cord tissue. Immunohistochemistry and Western blot methods were used to detect the expression of proteins Delta1, Presenilin1, Hes1, and Hes5 in the injured spinal cord.
The results showed that the expression levels of Delta1, Presenilin1, Hes1, and Hes5 increased significantly after spinal cord injury and decreased after electroacupuncture treatment. Our study suggested that the possible mechanism by which electroacupuncture could benefit the recovery after spinal cord injury in rats may include inhibiting the Notch signaling pathway and regulating the downstream proteins expression.
In addition, our study can provide reference for selecting acupoints and treatment cycle in the treatment of spinal cord injury .
Reference: https://pubmed.ncbi.nlm.nih.gov/34636492/