| Objective:Currently there is no ideal animal model for chronic cervical spinal cord compression. This experiment designed and synthesized a new chronic water-absorbing material, which was implanted into the spinal canal of rats to simulate pathogenesis of cervical spondylotic myelopathy. Studying the expression of the mammalian target of rapamycin(m Tor) and intramedullary apoptosis in the animal model, this experiment explored the role of m Tor and apoptosis in spinal cord injury and repair process. Methods:Male SD rats implanted with the water-absorbing material through posterior approach operation were divided into experimental group, while rats with removing the material immediately after implantation were divided into control group. There were 15 rats in each group. BBB score was evaluated everyday after surgery. MRI was tested in the 1day, 3day, 7day, 10 day and 14 day respectively after surgery. The rats were then sacrificed and the compressed lesion in spinal cord was made into tissue sections. HE staining, TUNEL staining, and immunohistochemistry for m Tor were performed thereafter. Results:BBB score of all rats were back to normal 3 days after surgery. MRI showed progressive spinal cord compression. HE staining showed intramedullary edema and vacuolar degeneration. Loss of motor neurons were more obvious in dorsal horn. TUNEL staining showed apoptosis were significant higher in every time point after surgery than control group. Immunohistochemistry showed m Tor positive cells reached top at 7 day after surgery and were statistically different compared to control group. Conclusions:Continuous compression can triger m TOR signaling pathway, which has neuroprotective function and helps the recovery of spinal cord, but the exact mechanism is different in acute phase and chronic phase. Severe apoptosis are not seen in slight compression of spinal cord, and the spontaneous repairment of spinal cord has certain effects in the process of neural function recovery. |
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