实验性过敏性脑脊髓炎中枢神经系统中NF-κB p65的免疫组化研究  

Expression of Transcription Factor NF-kB p65 in CNS of Experimental Allergic Encephalomyelitis

作　　者：于国平[1] 朱克[1] 田东华[1] 周湘军 

机构地区：[1]解放军总医院神经内科,北京100853

出　　处：《中国神经免疫学和神经病学杂志》1998年第1期16-20,共5页Chinese Journal of Neuroimmunology and Neurology

摘　　要：目的探索核转录因子NF－κB在中枢神经系统炎性脱鞘病发病中的作用。方法用牛脊髓髓鞘碱性蛋白加完全福氏佐剂对豚鼠进行免疫，诱发多发性硬化症的经典性动物模型——实验性过敏性脑脊髓炎（EAE）。并采用免疫组化方法对EAE中枢神经系统中核转录因子（NF）-κBp65的表达进行了研究。结果在EAE急性期血管周围浸润细胞和活化的小胶质细胞样细胞呈现NF－κBp65免疫反应阳性，而恢复期这种免疫反应明显减弱。结论EAE致炎性基因的表达可能与转录因子NF－κBp65的诱导有关。Objective To investigate the role of NF-K B in the pathogenesis of demyelinating diseases of central nervous system. Methods Experimental allergic encephalomyelitis (EAE)in guinea pigs were induced by using MBP (n=30) and the expression of NF-k B p65 in central nervous systern of EAE were revealed by immunohistochemical technique in this study.For demonstrating the microglia and astrocytes, the antibodies against RCA-1 and GFAPwere used. Results Immunohistochernical reactivity for the DNA-binding subunit p65 wasgenerally low and restricted to the surface of small to medium-sized blood vessels in the CNSin control group. Slight immunohistochemical reactivity in cells were detected at the 3 daysbefore appearance of clinical symptoms. At initial and peak stages of EAE, the immunohistochemical reactivity became strong. At the recovery stage of EAE, p65 immunoreactivityhad declined to base line levels. Within the resident glial cell population, p65 immunohistochemical reactivity cells were identified as RCA-1 positive microglia. GFAP- positive astrocytes did not show significant p65 immunohistochemical reactivity. The result suggests acrucial involvement of the transcription factor NF-K B p65 in autoimmune diseases of CNS.Furthermore, NF-K B p65 might be used as a marker for inflammatory processes.

关 键 词：脑脊髓炎 核转录因子 免疫组织化学 脱髓鞘疾病 

分 类 号：R744.5[医药卫生—神经病学与精神病学] R446.61[医药卫生—临床医学]