The Influence Of The Inhibitors Of MEK On Glial Scar Formation After Acute Spinal Cord Injury

Objective To observe the influence of the inhibitors of MEK on glial scar formation after acute spinal cord injury in a rat model.To study the mechanism of the formation of glial scar.Methods Thirty-six adult female Sprague-Dawley rats were divided randomly into sham injury group (A group,n=12), SCI group (B group,n=12), and U0126 treatment group(C group, n=12).All animals were anesthetized with amobarbital sodium (30mg/kg) and SCI lesions were made at T12 segment of spine with modified Allen's impact device in group B and C, which were contused by 70gcf(10g×7cm) energy respectively,following T12 laminectomy. The sham injury group only accepted the pseudo-operation. Locomotor capacity was assessed according to the 21-point Basso,Beattie and Bresnahan score at the minute,1d,3d,5d,7d,14d, 21d, and 28d after injury. Somatosensory evoked potential were used to assess neurologic recovery.While the lesions were obtained and studied by conventional histology,GFAP and Vim immunohistochemistry(HIC) using light microscopy at 14d and 28d after injury.The date was managed by the SPSS 16.0 software.Results 1.The rats had significant deficits in hind limb movement after spinal cord injury, according to the modified BBB hind limb locomotor rating scale score and Somatosensory evoked potential.U0126 treatment improved the hind limb motor function(P<0.05).2.Spinal cord injury resulted in astrocyte acitivation,and proliferation and increased expression of GFAP and Vim,leading eventually to the formation of glial scar.U0126 treatment down-regulated expression of GFAP and Vim(P<0.05),and reduced the formation of glial scar.Conclusion 1.The glial scar model which is made with modified Allen's method by 70gcf(10g×7cm) energy is effect and feasible.2.The inhibitors of MEK can improve the hindlimb motor function.3.The inhibitors of MEK can reduce the formation of the glial scar by suppressing the proliferation of astrocyte.