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Effect of NT-3 on repair of spinal cord injury through the MAPK signaling pathway.

OBJECTIVE
The aim of this study was to explore the effect of neurotrophin-3 (NT-3) on the repair of spinal cord injury (SCI) through the mitogen-activated protein kinase (MAPK) signaling pathway.


MATERIALS AND METHODS
The rat model of SCI was first successfully established using the impactor (SCI group). Meanwhile, control group and NT-3 treatment group were set up as well. Basso-Beattie-Bresnahan (BBB) score was given and blood, and spinal cord tissues were collected from rats. Subsequently, serum indexes were detected, including glucose (Glu), creatinine (Cr), K+, Na+, the content of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-β (TNF-β), and the level of myeloperoxidase (MPO). Moreover, the morphological changes were observed via hematoxylin-eosin (HE) staining. The gene and protein expressions of glial fibrillary acidic protein (GFAP) and MAPK were determined through Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting, respectively. Furthermore, the effect of the MAPK signaling pathway on SCI was comprehensively observed.


RESULTS
In SCI group, the rats could not crawl autonomously with the loss of motor function and paraplegia. Meanwhile, the levels of Glu, Cr, Na+, IL-6, IL-1β, TNF-β, and MPO were all significantly up-regulated. According to the results of HE staining, spinal nerve fibers disappeared with significant syringomyelia in SCI group. Meanwhile, the aggregation of nerve fibers was observed without apparent tissue bleeding, edema, and cell deformation in NT-3 group. QRT-PCR results demonstrated that SCI group showed remarkably higher levels of GFAP, MAPK, and c-Jun N-terminal kinase (JNK) (p<0.05), while it showed a markedly lower level of ERK2 than NT-3 group (p<0.05). In NT-3 group, the protein expression of MAPK in myocardial tissues was remarkably lower than that of SCI group (p<0.05).


CONCLUSIONS
NT-3 can inhibit the MAPK signaling pathway, thereby promoting the repair of SCI.