Aggravation Of Spinal Cord Injury By Ccl5 Via Activating Nk-Kappa B Signaling Pathway

The prognosis of spinal cord injury (SCI) is still unfavorable even under rapid progression of medicine. Due to the loss of regeneration potency of mature neurons, lots of SCI patients suffer from severe motor and/or sensory dysfunctions. Chemokines are closely correlated with SCI as inflammation related factors. This study thus investigated the role and mechanism of chemokines in SCI. A total of 30 SD rats were prepared for SCI model, in parallel with 30 SD rats recruiting sham control group. The successful generation of SCI model was examined by motor dysfunction scale. Microarray assay screened out those cytokines with significant changes between groups, followed by qPCR confirmation. Primary neurons from both groups were treated with recombinant CCL5 protein. Pathway Finder was used to screen out those signal pathways with significant change, followed by confirmation by immunofluorescence assay. The generation of SCI model was evaluated by motor dysfunction scale, which showed significantly lowered motor score in model group compared to sham group, suggesting successful generation of SCI model. Both microarray chip and qPCR reveled over-expression of CCL5 in SCI tissues (P=0.025). Primary culture of neurons treated with CCL-5 revealed activation of NK-kappa B and nuclear translocation of pP65 by immunofluorescence assay, but not in DMSO control group. CCl5 is over-expressed after SCI, and may aggravate SCI via activating NK-kappa B signal pathway.