ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of suppressing apoptosis signal regulating kinase 1 (ASK1) on glial fibrillary acidic protein (GFAP) and vimentin expressions at the injury site and on hindlimb mobility in rats after spinal cord injury (SCI).</p><p><b>METHODS</b>The rat models of SCI were established by extradural compression of the spinal cord using an aneurysm clip. The injured rats were treated with normal saline (model group), ASK1 specific inhibitor thioredoxin (Trx group), or ASK1 monoclonal antibody (Anti-ASK1 group), and the rats receiving a sham operation underwent laminectomy without SCI. The expression of GFAP and vimentin were detected by Western blotting and immunofluorescence assay at 1, 7, 14 and 28 days after SCI. The motion function of the hindlimbs of the injured rats was assessed with Basso Beattie Bresnahan (BBB) scores, and somatosensory-evoked potentials (SEP) and motor-evoked potentials (MEP) were determined to examine the electrophysiological changes.</p><p><b>RESULTS</b>At 1 day after SCI, the expressions of GFAP and vimentin showed no significant differences among the groups; at 7, 14 and 28 days after SCI, GFAP and vimentin expressions significantly increased in Trx and Anti-ASK1 groups compared with those in the model group (P<0.01). The BBB scores showed no significant differences among the groups at 1, 7 and 14 days after SCI, while at 28 days, the BBB scores in Trx and Anti-ASK1 groups were significantly higher than those in the model group (P<0.01). At 28 days after SCI, the latent period of SEP and MEP decreased and the amplitude increased significantly in Trx and Anti-ASK1 groups compared with that in the model group (P<0.01).</p><p><b>CONCLUSION</b>Blocking ASK1 can inhibit the expression of GFAP and vimentin in glial scars and improve the outcomes of hindlimb mobility in rats after SCI.</p>