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Objective: To explore the protective effect and mechanism of neomycin A (CsA) on rat spinal cord injury (SCI) early cyclosporine. Methods: Rat SCI experimental animal models. 180 rats were randomly divided into control group, injury group and injury CsA-treated group, n = 60. Respectively modeling at different time points were sacrificed, intubation, spinal cord injury drawn, fixed overnight, embedded, sliced. The samples were HE staining, immunohistochemistry EnVision method to detect the expression of TNF-a, immunohistochemistry SP method Cox-2 expression. Using HPIAS-2000 high-definition Color pathology report management system for quantitative analysis of TNF-a and Cox-2 expression. Results: HE staining under light microscope observation: visible white matter, gray matter and gray matter in the anterior horn and posterior horn of the spinal cord of normal rats. CsA treatment group in the injury group and injury within 6 hours after injury spinal cord hemorrhage, no necrosis. With time in the spinal cord injury group wide range of focal hemorrhage and bleeding after the formation of cysts, a large number of neuron degeneration and necrosis, dissolved proliferation of glial cells and neutrophil infiltration. With time after injury CsA treatment group spinal cord focal hemorrhage, swelling of the neurons, nerve cell degeneration and necrosis, hemorrhage, proliferation of glial cells and infiltration of inflammatory cells than those in the light of the injury group. 2, Cox-2 in normal rats spinal cord was suspicious expression, injury group was strongly positive expression in rat spinal cord, CsA treatment group was weakly positive expression in rat spinal cord injury. 2h injury group after injury and injury CsA treatment group that is the expression of Cox-2; damage after 6h Cox-2 reached the peak, but the peak short duration; damage after 48h Cox-2 expression decreased to near baseline levels drop 72 hours to baseline levels. Three groups at each time point of the image analysis results by single-factor analysis of variance, the difference was statistically significant (2h: F = 179.670, P <0.001; 6h: F = 337.489, P <0.001; 12h: F = 393.312, P <0.001 ; 24h: F = 197.541, P <0.001; 48h: F = 35.174, P <0.001; 72h: F = 3.995, P = 0.030). 3, TNF-a in normal rats spinal cord was suspected positive or weakly positive, strong expression injury in rats spinal cord injury, CsA treatment group was moderate expression in rat spinal cord. 2h injury group after injury and injury CsA treatment group that is the expression of TNF-a; damage after 12h TNF-a reached the peak, but the peak short duration; damage 72 hours after TNF-a expression decreased to baseline levels. Three groups at each time point image analysis results by the single factor variance analysis, group significant difference (2h: F = 300.328, P <0.001; 6h: F = 1856.199, P <0.001; 12h: F = 3710.988, P < 0.001; 24h: F = 2516.988, P <0.001; 48h: F = 647.982, P <0.001; 72h: F = 3.454, P = 0.046). Conclusion: CsA could significantly reduce the Cox-2 and TNF-a expression in spinal cord tissue after SCI, CSA can reduce spinal cord injury, have a therapeutic effect on the secondary SCI.
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