Bellander B M, von Holst H, Fredman P, Svensson M
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
J Neurosurg. 1996 Sep;85(3):468-75. doi: 10.3171/jns.1996.85.3.0468.
The aim of the present study was to examine the glial cell response and the possible involvement of the complement cascade following a cerebral cortical contusion. The lesion was produced using a standardized weight-drop technique in adult rats. The blood-brain barrier was damaged, as demonstrated by a decrease of immunoreactivity for a tight junction protein normally expressed by endothelial cells of small vessels in the central nervous system. Increased immunoreactivity for microglial (OX42) and astroglial cells (glial fibrillary acidic protein), as well as macrophages expressing ED1-immunoreactivity (IR) were found in the vicinity of the lesion at all postoperative survival times (2-14 days). In the present study complement factor C3d- and C9-IR was found around the lesion, indicating that activation of the complement cascade had taken place. Furthermore, immunoreactivity for the putative complement inhibitor clusterin (sulfated glycoprotein-2) was found in some of the injured neurons. The contralateral hemisphere showed no evidence of the reaction found in the ipsilateral hemisphere. The balance between complement activation and complement inhibitors may have an impact on the degenerative components in the brain following traumatic injury and in particular on the events leading to nerve cell death.
本研究的目的是检查大脑皮质挫伤后胶质细胞的反应以及补体级联反应可能的参与情况。采用标准化的重物坠落技术在成年大鼠身上制造损伤。血脑屏障受到破坏，这可通过中枢神经系统中小血管内皮细胞正常表达的紧密连接蛋白免疫反应性降低来证明。在所有术后存活时间（2 - 14天），在损伤部位附近均发现小胶质细胞（OX42）和星形胶质细胞（胶质纤维酸性蛋白）的免疫反应性增加，以及表达ED1免疫反应性（IR）的巨噬细胞。在本研究中，在损伤部位周围发现补体因子C3d和C9免疫反应性，表明补体级联反应已经发生。此外，在一些受损神经元中发现了假定的补体抑制剂簇集蛋白（硫酸化糖蛋白-2）的免疫反应性。对侧半球未显示出在同侧半球发现的反应迹象。补体激活与补体抑制剂之间的平衡可能会影响创伤性脑损伤后大脑中的退行性成分，特别是对导致神经细胞死亡的事件产生影响。
