Beattie Michael S
Spinal Trauma and Repair (STAR) Laboratories, Neurobiology of Disease Institute and Department of Neuroscience, The Ohio State University Medical Center, Columbus, OH 43210, USA.
Trends Mol Med. 2004 Dec;10(12):580-3. doi: 10.1016/j.molmed.2004.10.006.
The secondary cascade of cell death that follows central nervous system (CNS) injury or ischemia has long been considered a target for neuroprotective agents aimed at sparing tissue and function. Recently, several laboratories have shown remarkable protection and recovery of function in rodent models of spinal cord injury using treatments that target components of the CNS inflammatory response. The use of minocycline, an antibiotic that reduces microglial activation, antibody blockade of the CD95 (FAS) ligand and the blockade of glycosphingolipid-induced iNOS (inducible nitric oxide synthase) have recently been shown to reduce neuronal and glial apoptosis with concomitant improvement in neurological function, and appear to enhance the efficacy of cell transplantation strategies.
长期以来，中枢神经系统（CNS）损伤或缺血后发生的继发性细胞死亡级联反应一直被视为旨在保护组织和功能的神经保护剂的作用靶点。最近，几个实验室在脊髓损伤的啮齿动物模型中，使用针对CNS炎症反应成分的治疗方法，显示出显著的组织保护和功能恢复。最近的研究表明，使用米诺环素（一种可减少小胶质细胞激活的抗生素）、CD95（FAS）配体的抗体阻断以及糖鞘脂诱导的诱导型一氧化氮合酶（iNOS）的阻断，可减少神经元和神经胶质细胞的凋亡，同时改善神经功能，并且似乎能提高细胞移植策略的疗效。
