| Objective:1.To establish an ideal, practical chronic spinal cord compression model for exploring the pathophysiology of chronic compressive spinal cord injury (CCSCI) and lay the foundation. At the L3-L4segment of the spinal cord in the model subdural catheter, catheter at the muscle and subcutaneous fixed extension tube fixed in vitro and plugging in vitro controllability extend and Tube for injecting drug use.2.By paclitaxel (Taxol) on rat CCSCI after spinal cord tissue pathological changes, proliferation of astrocytes, glial scar formation, the role of recovery of neurological function, and explore Taxol in chronic spinal cord injury in rats and its possible mechanism to provide a theoretical basis for clinical treatment.Method:1. Rat model:we choose56female Wistar rats which are randomly divided into experimental group (n=48) and control group (C, n=8), the experimental group animals the chest posterior laminectomy, the drawer tail hook (drawer-hook, D-H) spinal cord compression device implanted between T8-T10. Every7days we screw into one week (0.5mm), up to four weeks, screws through a steel gasket pressure on the spinal cord, after1week rats were anesthetized, the thoracic spine is examined by lateral X-ray, evaluated device the position and thoracic spinal stenosis. The animals of the control group is experimented by only posterior laminectomy, hind limb motor function in the first4weeks after the Basso Beattie Bresnahan (BBB) score. Except for acute spinal cord injury in animals.2.48has produced successful rat model of chronic spinal cord compression, line intrathecal catheter model is created using a random number table which is divided into Taxol treatment group (A, n=24), the chronic compression group (B, n=24). The A group was given Taxol intrathecal injection. Each group at each time point of8,14,21,28days after chronic compressive spinal cord injury BBB rating, evaluation of the functional status of the spinal cord. Select two each of the three groups of rats after the amount of anesthesia directly killed TTC staining spinal cord blood flow changes in the first four weeks. The remaining six rat spinal cord specimens were pathologically technology line HE, TUNEL and immunohistochemical staining was observed pressure pathological changes detected in the spinal cord cell apoptosis and GFAP expression in the spinal cord. A group and B group compared and analyzed statistically. In order to facilitate control, the other two of normal rats, TTC staining of a line, a line of pathological staining.Results:1.X-ray shows great compression device location, the exact spinal cord is compressed. In line with the requirements of the posterior chronic progressive compression model device.2.Taxol treatment group,21and28days of hindlimb motor function Basso Beattie Bresnahan (BBB) scores were significantly better than the the chronic compression group (p<0.05). Animal BBB score, the28d the treatment group compared with the control group has no significant decrease (p=0.316).3.The TTC staining is observed spinal cord ischemia position:normal rat spinal cord cross-section of a good blood supply;21,28days Taxol in the treatment group compared to the chronic compression group, the cross-section of the rat spinal cord white matter of spinal cord compression side white in color area is relatively small.4.Spinal cord specimens HE staining:chronic compression-of the spinal cord gray matter is loss of neurons, there are the irregular sheet demyelinating area gliosis. Using Taxol treatment for14days, comparing with the more complete form of spinal cord compression group, neuronal shrinkage, showing dissolved necrosis alleviate mild inflammatory response. After CCSCI,28d, with Taxol after treatment, spinal cord tissue structure shows more clear, more normal neurons. Tip Taxol after spinal cord injury can reduce the glial scar formation, contribute to the regeneration of axons through the glial scar zone, create a new neural pathways and functional linkages; which proves that the number of positive apoptosis by TUNEL staining and The oppression Time be positively correlated.5.Immunohistochemical staining:21d Taxol treatment groups oppressed the edge of the central area of GFAP staining weakened to vary degrees, decreased expression, including Taxol treatment group increased with time, the inhibitory effect of increase indicating that Taxol can inhibit spinal cord injury. GFAP expression weaken the barrier function of the glial scar, which is conducive to the regeneration of axons. Early application of Taxol treatment after spinal cord injury can inhibit the increase in the damage zone around the spinal cord tissue expression of GFAP.6.21d,28d Taxol treatment group the number of GFAP-positive cells were26.50±2.43,21.33±2.25, chronic compression of GFAP positive cells to35.00±3.16,38.00±5.44, groups were significantly different (p<0.05).Conclusion:1.This device simulate the clinical features of chronic progressive spinal cord compression, chronic spinal cord compression is an ideal and practical model complyed with the requirements of the posterior chronic progressive compression model device. Intrathecal catheter model in rats can reduce the damage in rats, reducing the requirement of experimental animals which has a good effect.2.Taxol promote CCSCI after hindlimb motor function recovery;and injury site can inhibit the generation of the intermediate filament protein marker GFAP, weaken astrocytes reactive gliosis, reduce glial scar formation, due to glial scarring caused by physical and chemical barrier.Taxol can inhibit the inflammatory response the local microenvironment improve CCSCI after injury, which play a role in the protection of nerve cells. |
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