Aronica E, Boer K, van Vliet E A, Redeker S, Baayen J C, Spliet W G M, van Rijen P C, Troost D, da Silva F H Lopes, Wadman W J, Gorter J A
Department of (Neuro) Pathology, Academic Medical Center, University of Amsterdam, The Netherlands.
Neurobiol Dis. 2007 Jun;26(3):497-511. doi: 10.1016/j.nbd.2007.01.015. Epub 2007 Feb 20.
We investigated the involvement of the complement cascade during epileptogenesis in a rat model of temporal lobe epilepsy (TLE), and in the chronic epileptic phase in both experimental as well as human TLE. Previous rat gene expression analysis using microarrays indicated prominent activation of the classical complement pathway which peaked at 1 week after SE in CA3 and entorhinal cortex. Increased expression of C1q, C3 and C4 was confirmed in CA3 tissue using quantitative PCR at 1 day, 1 week and 3-4 months after status epilepticus (SE). Upregulation of C1q and C3d protein expression was confirmed mainly to be present in microglia and in a few hippocampal neurons. In human TLE with hippocampal sclerosis, astroglial, microglial and neuronal (5/8 cases) expression of C1q, C3c and C3d was observed particularly within regions where neuronal cell loss occurs. The membrane attack protein complex (C5b-C9) was predominantly detected in activated microglial cells. The persistence of complement activation could contribute to a sustained inflammatory response and could destabilize neuronal networks involved.
我们研究了补体级联反应在颞叶癫痫（TLE）大鼠模型癫痫发生过程中以及在实验性和人类TLE慢性癫痫阶段的作用。先前使用微阵列进行的大鼠基因表达分析表明，经典补体途径显著激活，在癫痫持续状态（SE）后1周时，在CA3区和内嗅皮质达到峰值。使用定量PCR在癫痫持续状态（SE）后1天、1周和3 - 4个月时，证实CA3组织中C1q、C3和C4的表达增加。C1q和C3d蛋白表达上调主要在小胶质细胞和少数海马神经元中被证实存在。在伴有海马硬化的人类TLE中，特别是在神经元细胞丢失发生的区域内，观察到星形胶质细胞、小胶质细胞和神经元（5/8例）表达C1q、C3c和C3d。膜攻击蛋白复合物（C5b - C9）主要在活化的小胶质细胞中被检测到。补体激活的持续存在可能导致持续的炎症反应，并可能使相关的神经元网络不稳定。
