Stroke induces histamine accumulation and mast cell degranulation in the neonatal rat brain
Stroke induces histamine accumulation and mast cell degranulation in the neonatal rat brain
复制标题
DOI：
10.1111/j.1750-3639.2007.00092.x
复制
发表时间：
2008-01-01
期刊：
影响因子：
6.4
通讯作者：
Heron, A.
中科院分区：
文献类型：
--
作者：
Biran, V.;Cochois, V.;Heron, A.
炎症过程是缺氧缺血性脑损伤的主要原因。本研究主要关注P7新生大鼠永久性左大脑中动脉和同侧短暂性颈总动脉闭塞（50分钟）引起的暂时性局灶性缺血模型中脑组胺系统和肥大细胞的变化。免疫组织化学分析显示，缺血诱导组胺（HA）在缺血后6-12小时的梗死核心和24-48小时的半暗区积累，尽管原位杂交未能在这些区域检测到任何组氨酸脱羧酶基因转录物。HA与MAP2标记物的免疫组化共定位显示，HA在神经元细胞变性前就已在细胞内积累，并且在再灌注12 h和48 h时肥大细胞数量显著增加。在肥大细胞中，组胺免疫反应性在缺血后2、6和12小时检测到，而在缺血后24小时，组胺免疫反应性消失，此时肥大细胞同时出现脱颗粒。综上所述，这些数据表明，释放组胺的脑肥大细胞的募集可能有助于未成熟脑缺血诱导的神经元死亡。
Inflammatory processes are a major cause of hypoxic-ischemic brain damage. The present study focuses on both the cerebral histamine system and mast cells in a model of transient focal ischemia induced by permanent left middle cerebral artery, and homolateral transient common carotid artery occlusion (50 minutes) in the P7 newborn rat. Immunohistochemical analysis revealed that ischemia induces histamine (HA) accumulation in the core of the infarct 6-12 h post-ischemia, and in the penumbra at 24-48 h, although in situ hybridization failed to detect any histidine decarboxylase gene transcripts in these regions. Immunohistochemical co-localization of HA with the MAP2 marker revealed that HA accumulates in neuronal cells before they degenerate, and is accompanied by a very significant increase in the number of mast cells at 12 h and 48 h of reperfusion. In mast cells, histamine immunoreactivity is detected at 2, 6 and 12 h after ischemia, whereas it disappears at 24 h, when a concomitant degranulation of mast cells is observed. Taken together, these data suggest that the recruitment of cerebral mast cells releasing histamine may contribute to ischemia-induced neuronal death in the immature brain.