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The aim of this study was to investigate the effect of U0126 on the formation of glial scars following spinal cord injury (SCI) in a rat model. Ninety adult female Sprague-Dawley rats were divided randomly into sham injury (group I), SCI (group II) and U0126 treatment (group III) groups, and functional outcome was observed during the 4 weeks following the injury. The P1 and N1 latencies and P1-N1 amplitudes of somatosensory-evoked potentials (SEPs) were collected one day prior to surgery, on the day of surgery and 14 and 28 days postoperatively. The expression levels of glial fibrillary acidic protein (GFAP) and vimentin (Vim) were assessed 14 and 28 days post-injury. Treatment with U0126 significantly increased locomotor function from the second week until 4 weeks post-SCI. At 14 and 28 days subsequent to the injury, the number of cells that were positive for GFAP expression in the U0126-treated group was significantly reduced and the GFAP-positive cells were observed to be smaller, with a reduced prominence and pale staining. Moreover, the area of glial scarring was smaller compared with that of the SCI controls. Inhibitors of MEK may reduce glial scar formation by suppressing the proliferation of astrocytes, and may improve hindlimb motor function.

MEK inhibition reduces glial scar formation and promotes the recovery of sensorimotor function in rats following spinal cord injury