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本文引用的文献

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Analysis of FK506-mediated protection in an organotypic model of spinal cord damage: heat shock protein 70 levels are modulated in microglial cells.FK506介导的脊髓损伤器官型模型中的保护作用分析:小胶质细胞中热休克蛋白70水平受到调节。
Neuroscience. 2008 Jul 31;155(1):104-13. doi: 10.1016/j.neuroscience.2008.04.078. Epub 2008 Jun 5.
2
Spinal cord injury--scientific challenges for the unknown future.脊髓损伤——未知未来的科学挑战。
Ups J Med Sci. 2007;112(3):259-88. doi: 10.3109/2000-1967-200.
3
Increased chondroitin sulfate proteoglycan expression in denervated brainstem targets following spinal cord injury creates a barrier to axonal regeneration overcome by chondroitinase ABC and neurotrophin-3.脊髓损伤后去神经支配的脑干靶点中硫酸软骨素蛋白聚糖表达增加,形成了轴突再生的障碍,而软骨素酶ABC和神经营养因子-3可克服这一障碍。
Exp Neurol. 2008 Feb;209(2):426-45. doi: 10.1016/j.expneurol.2007.03.029. Epub 2007 Apr 12.
4
Cyclosporin-A enhances non-functional axonal growing after complete spinal cord transection.环孢素A可促进脊髓完全横断后无功能轴突的生长。
Brain Res. 2007 May 29;1149:200-9. doi: 10.1016/j.brainres.2007.02.056. Epub 2007 Mar 1.
5
Transplantation of fibroblasts that overexpress matrix metalloproteinase-3 into the site of spinal cord injury in rats.
J Neurotrauma. 2006 Dec;23(12):1750-65. doi: 10.1089/neu.2006.23.1750.
6
Protective effect of cyclosporin-A in spinal cord injury: an overview.
Curr Med Chem. 2006;13(22):2703-10. doi: 10.2174/092986706778201503.
7
Adult neural stem cells and central nervous system repair.成体神经干细胞与中枢神经系统修复。
Ernst Schering Res Found Workshop. 2006(60):215-28. doi: 10.1007/3-540-31437-7_14.
8
Fate of endogenous stem/progenitor cells following spinal cord injury.脊髓损伤后内源性干细胞/祖细胞的命运
J Comp Neurol. 2006 Oct 1;498(4):525-38. doi: 10.1002/cne.21065.
9
Endothelial cell loss is not a major cause of neuronal and glial cell death following contusion injury of the spinal cord.脊髓挫伤损伤后,内皮细胞丢失并非神经元和神经胶质细胞死亡的主要原因。
Exp Neurol. 2006 Nov;202(1):8-20. doi: 10.1016/j.expneurol.2006.05.028. Epub 2006 Jul 26.
10
Neurological aspects of spinal-cord repair: promises and challenges.脊髓修复的神经学方面:前景与挑战。
Lancet Neurol. 2006 Aug;5(8):688-94. doi: 10.1016/S1474-4422(06)70522-1.

环孢素 A 对挫伤性脊髓损伤后功能恢复的影响。

Effect of cyclosporin A on functional recovery in the spinal cord following contusion injury.

机构信息

Department of Anatomy, National University of Ireland, Galway, Ireland.

出版信息

J Anat. 2009 Sep;215(3):267-79. doi: 10.1111/j.1469-7580.2009.01107.x. Epub 2009 Jun 24.

DOI:10.1111/j.1469-7580.2009.01107.x
PMID:19558472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2750760/
Abstract

Considerable evidence has shown that the immunosuppressant drug cyclosporin A (CsA) may have neuroprotective properties which can be exploited in the treatment of spinal cord injury. The aim of this study was to investigate the cellular environment within the spinal cord following injury and determine whether CsA has an effect on altering cellular interactions to promote a growth-permissive environment. CsA was administered to a group of rats 4 days after they endured a moderate contusion injury. Functional recovery was assessed using the Basso Beattie Bresnahan (BBB) locomotor rating scale at 3, 5 and 7 weeks post-injury. The rats were sacrificed 3 and 7 weeks post-injury and the spinal cords were sectioned, stained using histological and immunohistochemical methods and analysed. Using stereology, the lesion size and cellular environment in the CsA-treated and control groups was examined. Little difference in lesion volume was observed between the two groups. An improvement in functional recovery was observed within CsA-treated animals at 3 weeks. Although we did not see significant reduction in tissue damage, there were some notable differences in the proportion of individual cells contributing to the lesion. CsA administration may be used as a technique to control the cell population of the lesion, making it more permissive to neuronal regeneration once the ideal environment for regeneration and the effects of CsA administration at different time points post-injury have been identified.

摘要

大量证据表明,免疫抑制剂环孢素 A(CsA)可能具有神经保护特性,可用于治疗脊髓损伤。本研究旨在探讨损伤后脊髓内的细胞环境,并确定 CsA 是否会影响细胞相互作用,以促进有利于生长的环境。CsA 在大鼠经历中度挫伤伤后 4 天给予一组大鼠。使用 Basso Beattie Bresnahan(BBB)运动评分量表在损伤后 3、5 和 7 周评估功能恢复。大鼠在损伤后 3 和 7 周处死,脊髓切片,用组织学和免疫组织化学方法染色并进行分析。使用立体学,检查 CsA 处理组和对照组的病变大小和细胞环境。两组之间的病变体积差异不大。在 3 周时,CsA 处理的动物的功能恢复有所改善。虽然我们没有看到组织损伤的显著减少,但在导致病变的单个细胞的比例上存在一些明显的差异。CsA 的给药可以用作控制病变细胞群体的技术,一旦确定了再生的理想环境以及 CsA 在损伤后不同时间点给药的效果,就可以使病变更有利于神经元再生。