动物实验 z-bo 2020-08-22 569

　　Objective: To investigate the expression of apoptosis signal regulatory protein 1 (ASK1) in glial scars after spinal cord injury (SCI), its protein, glial fibrillary acidic protein (GFAP) and vimentin (vimentin) Damage to the hind limbs of the rat.

　　Methods: Using rat spinal cord injury model, ASK1 specific inhibitor thioredoxin group (Trx group), ASK1 monoclonal antibody group (anti-ASK1 group), saline control group (model group) and sham operation group (sham operation) ) Immediately after injury, thioredoxin, 10μl of ASK1 monoclonal antibody and 10μl of saline were injected into the injured site. Rats in the sham operation group opened their pedicles to expose the spinal cord, without causing spinal cord injury. Rats in each group routinely (1, 7, 14, 28 days after SCI) used Western blot, immunofluorescence and BBB score to detect the behavioral changes of rat hindlimbs to detect the expression of GFAP and vimentin. Varieties that use somatosensory and motor evoked potentials to detect and detect electrophysiological effects.

　　Result: One day after SCI, there was no significant difference in the expression of GFAP and vimentin in each group. The expressions of GFAP and vimentin in the 7, 14, 28 dTrx group and anti-ASK1 group were significantly lower than those in the model group (P\u003c0.01); SCI 1, 7 and BBB scores after somatosensory induction on day 14, the potential and There were no significant differences in motor evoked potentials. At 28 days after SCI, the BBB scores of Trx and Anti-ASK1 groups were significantly higher than those of the model group (P\u003c0.01), somatosensory and motor evoked potentials were significantly shortened, and the incubation period reached the peak. This value has increased significantly (P\u003c0.01 or P\u003c0.01).

　　Conclusion: Inhibition of ASK1 can attenuate the expression of GFAP and vimentin in SCI glial scars in rats, and promote the recovery of hindlimb motor function and the improvement of rat electrophysiology.