Tomimoto H, Yamamoto K, Homburger H A, Yanagihara T
Department of Neurology, Mayo Clinic, Rochester, MN 55905.
Acta Neuropathol. 1993;86(5):447-55. doi: 10.1007/BF00228579.
Alteration of creatine kinase BB-isoenzyme (CK-BB) was investigated in the vulnerable CA1 region of the hippocampus of ischemic and postischemic gerbil brains using immunoelectron microscopy. CK-BB existed in the neuronal perikarya, dendrites and axons as well as in astroglias in the normal gerbil brain. Immunocytochemical reaction products were associated with microtubules and polyribosomes. Propagation of ischemic and postischemic damage with disintegration of microtubules was observed in the dendro-somatic direction in neurons, which progressed in parallel with dispersion and loss of the immunocytochemical reaction for CK-BB in the dendroplasm. After reperfusion for longer than 24 h, CK-BB was also observed in the extracellular space. The present result supported the notion that loss of the immunohistochemical reaction for CK-BB which has been observed by light microscopy after cerebral ischemia, was at least partly due to dispersion of this enzyme caused by disintegration of microtubules and extracellular leakage of this enzyme, although other processes, including degradation of CK-BB per se, were also possible. The loss of CK-BB from the neuronal structure may delay the recovery from ischemic damage and may eventually lead to neuronal death.
采用免疫电子显微镜技术,对缺血性和缺血后沙鼠脑海马CA1易损区肌酸激酶BB同工酶(CK-BB)的变化进行了研究。在正常沙鼠脑中,CK-BB存在于神经元胞体、树突和轴突以及星形胶质细胞中。免疫细胞化学反应产物与微管和多核糖体相关。在神经元中,观察到缺血和缺血后损伤沿树突-胞体方向传播,伴有微管解体,这与树突质中CK-BB免疫细胞化学反应的分散和丧失平行进展。再灌注超过24小时后,在细胞外间隙也观察到CK-BB。本研究结果支持以下观点:脑缺血后光镜下观察到的CK-BB免疫组化反应丧失,至少部分是由于微管解体导致该酶分散以及该酶的细胞外漏出,尽管包括CK-BB本身降解在内的其他过程也有可能。CK-BB从神经元结构中的丧失可能会延迟缺血损伤的恢复,并最终导致神经元死亡。