Lou J, Lenke L G, Ludwig F J, O'Brien M F
Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.
Spinal Cord. 1998 Oct;36(10):683-90. doi: 10.1038/sj.sc.3100632.
The complex biochemical interactions following acute spinal cord injury have undergone considerable investigation recently. Progress has been made in discovering both primary and secondary injury cascades that combine to produce the ultimate neurologic insult. Traditionally, neuronal and supporting cell death following spinal cord injury have focused on necrotic death pathways resulting passively from the actual mechanical tissue damage and inflammatory processes which follow. However, the occurrence of programmed apoptotic cell death which is an actively mediated cellular process may occur following acute spinal cord injury and, if present, may play a role in the ultimate neurologic insult. In this study, we document a chronologically-specific course of apoptotic cell death by the TUNEL assay technique following an acute experimental spinal cord injury in the rat model. In this manner, apoptotic cell death following acute spinal cord injury may play a pivotal role in the secondary injury cascade which produces the ultimate neurologic insult and may allow potential for mediating neuronal survival via anti-apoptotic factors such as the protooncogene Bcl-2.
急性脊髓损伤后的复杂生化相互作用近来已得到大量研究。在发现原发性和继发性损伤级联反应方面已取得进展，这些反应共同导致最终的神经损伤。传统上，脊髓损伤后神经元和支持细胞死亡一直聚焦于因实际机械性组织损伤及随后的炎症过程而被动产生的坏死性死亡途径。然而，程序性凋亡细胞死亡这种主动介导的细胞过程可能在急性脊髓损伤后发生，并且如果存在的话，可能在最终的神经损伤中起作用。在本研究中，我们通过TUNEL检测技术记录了大鼠模型急性实验性脊髓损伤后凋亡细胞死亡的时间特异性过程。通过这种方式，急性脊髓损伤后的凋亡细胞死亡可能在导致最终神经损伤的继发性损伤级联反应中起关键作用，并且可能为通过诸如原癌基因Bcl-2等抗凋亡因子介导神经元存活提供可能性。
