Department of Neuroscience and Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH 43210, USA.
PPAR Res. 2008;2008:517162. doi: 10.1155/2008/517162.
Traumatic injury to the spinal cord results in multiple anatomical, physiological, and functional deficits as a result of local neuronal and glial cell death as well as loss of descending and ascending axons traversing the injury site. The many different mechanisms thought to contribute to protracted secondary cell death and dysfunction after spinal cord injury (SCI) are potential therapeutic targets. Agents that bind and activate the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-gamma) show great promise for minimizing or preventing these deleterious cascades in other models of CNS disorders. This review will summarize the major secondary injury cascades occurring after SCI and discuss data from experimental CNS injury and disease models showing the exciting potential for PPARgamma therapies after SCI.
脊髓创伤会导致局部神经元和神经胶质细胞死亡，以及穿过损伤部位的下行和上行轴突丧失，从而导致多种解剖、生理和功能缺陷。许多不同的机制被认为导致脊髓损伤 (SCI) 后持续的继发性细胞死亡和功能障碍，这些机制可能成为治疗靶点。结合并激活转录因子过氧化物酶体增殖物激活受体-γ (PPAR-γ) 的药物在最小化或预防其他中枢神经系统疾病模型中的这些有害级联方面显示出巨大的潜力。这篇综述将总结 SCI 后发生的主要继发性损伤级联，并讨论来自实验性中枢神经系统损伤和疾病模型的数据，这些数据显示了 PPARγ 治疗 SCI 的令人兴奋的潜力。
