Abstract: Objective To explore p38 mitogen-activated protein kinase(p38MAPK) regulating glial fibrillary acidic protein(GFAP) and vimentin expressions at the early stage of glia scar formation after spinal cord injury in rats. Methods Rats were divided into sham group, model group, p38MAPK specific agonists group(anisomycin group) and p38MAPK specific inhibitor group(SB203580 group) randomly. Normal saline(model group), p38MAPK agonist anisomycin(anisomycin group), p38MAPK inhibitor SB203580(SB203580 group) every 10 ?L were respectively injected in the damaged area under spinal dura mater after the experimental model of SCI were created by extradural compression of the spinal cord using an aneurysm clip, and the sham group rats underwent laminectomy without SCI. The hind legs movement function of rats was evaluated by BBB scale on the 1st, 3rd, 7th and 14th day after SCI, and the the expressions of GFAP and vimentin were detected by western blotting and immunofluorescence assay. Results On the 14th day after SCI, the BBB scores of model group was significantly lower than that of sham group(p<0.01). the BBB scores of SB203580 group was significantly higher than that of model group(p<0.05), but was still lower than that of sham group(p<0.01), and the BBB scores of anisomycin group was significantly lower than that of model group(p<0.05). On the 7th and 14th day after SCI, the expressions of GFAP and vimentin in the model group was significantly higher than that in sham group(p<0.01). the expressions of GFAP and vimentin in SB203580 group was significantly lower than that in model group(p<0.05), but was still higher than that in sham group(p<0.05), and the expresssions of GFAP and vimentin in anisomycin group was significantly higher than that in model group(p<0.05). Conclusion p38MAPK can regulate the expressions of GFAP and vimentin at the early stage of glial scar formation after SCI. Inhibit p38MAPK can reduce the expressions of GFAP and vimentin, lighten glial scar formation after SCI in rats, promote the recovery of neural function.

Key words: spinal cord injury, p38 mitogen-activated protein kinase, GFAP, vimentin