[Exploration of the mechanism of electroacupuncture at "Jiaji" (EX-B2) in treating neuronal apoptosis in rats with spinal cord injury based on the JAK2/STAT3 pathway].

OBJECTIVES

To observe the effect of electroacupuncture (EA) at "Jiaji" (EX-B2) on inhibiting neuronal apoptosis in rats with spinal cord injury based on the Janus tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, so as to explore the underlying mechanism of EA in the treatment of spinal cord injury.

METHODS

A total of 36 SD rats were randomly divided into sham operation group, spinal cord injury group, and Jiaji EA group, with 12 rats in each group. The spinal cord injury model was established using Allen's method. The Jiaji EA group was treated with EA at EX-B2 (once a day, 30 min each time, for a total of 14 d). After the treatment, the Basso Beattie Bresnahan (BBB) score was used to evaluate the hindlimb motor function of rats in each group. HE staining was used to observe the morphological changes of spinal cord tissues. TUNEL staining was used to observe the pathological changes and neuronal apoptosis rate of the spinal cord. Western blot was used to detect the relative expression levels of phosphorylated (p)-JAK2, p-STAT3, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), and Caspase-3 proteins in the spinal cord.

RESULTS

Compared with the sham operation group at the same time point, the BBB score decreased (P<0.01), the spinal cord tissue structure in the injury area was disordered, the cell body shrank, and the neuronal apoptosis rate increased (P<0.01), the expression levels of p-JAK2, p-STAT3, Bax, and caspase-3 proteins increased (P<0.01) while the expression level of Bcl-2 protein decreased (P<0.01) in rats of the spinal cord injury group. Compared with the spinal cord injury group, the BBB score increased on the 7th and 14th day of intervention (P<0.01), the spinal cord tissue structure tended to be normal, the degree of neuronal damage was reduced, and the apoptosis rate decreased (P<0.01), the expression levels of p-JAK2, p-STAT3, Bax, and caspase-3 proteins decreased (P<0.01, P<0.05), while the expression level of Bcl-2 protein increased (P<0.05) in rats of the Jiaji EA group.

CONCLUSIONS

EA at EX-B2 can improve the motor function of rats with spinal cord injury, up-regulate the expressions of anti-apoptotic factors, down-regulate the expressions of pro-apoptotic factors, and reduce neuronal apoptosis in spinal cord injury. The mechanism may be related to the inhibition of the activation of the JAK2/STAT3 signaling pathway.