The cellular reactions to experimental intracerebral hemorrhage
The cellular reactions to experimental intracerebral hemorrhage
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DOI：
10.1016/0022-510x(95)00215-n
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发表时间：
1995-12-01
影响因子：
4.4
通讯作者：
McEvoy, JA
中科院分区：
文献类型：
--
作者：
Koeppen, AH;Dickson, AC;McEvoy, JA
脑出血的消退可以通过含铁血黄素的出现来衡量。血液外渗引起邻近存活组织中的细胞反应，其中损伤激活驻留的小胶质细胞并从血流中吸引更多的吞噬细胞。这种迁移到病灶周围反应区的信号尚未完全了解，但很可能是凝固血液中的蛋白质有助于细胞活化。为了研究血浆蛋白在病灶周围反应区发病机制中的作用，脑内注射自体全血在成年兔中制备0.1 ml或等体积的乳酸林格氏溶液中的洗涤的自体红细胞（RBC）。总铁量相同（30 μ g）。通过铁组织化学和铁蛋白、铁蛋白阻遏蛋白（FRP）、胶质细胞酸性蛋白（GFAP）和补体受体CR3的免疫细胞化学研究了对注射的细胞反应。实验性血肿在注射全血后比注射RBC后消退得慢得多。定性小胶质细胞和星形胶质细胞反应非常相似。然而，在48小时，注射全血后，铁和铁蛋白反应性小胶质细胞更多。注射后的任何一种类型，铁蛋白免疫反应细胞比铁阳性细胞更丰富。这一观察结果表明，全铁蛋白蛋白的生物合成和铁掺入独立进行。小胶质细胞表面CR3的表达在全血后更加突出，表明灭活的补体3b在吸引额外的吞噬细胞中的作用。在注射血液或RBC后5天开始转化为含铁血黄素。病变引起的星形胶质细胞在焦周区的初步破坏判断GFAP和FRP免疫反应。然而，在第5天，星形胶质细胞的过程重新进入周围区，并与小胶质细胞和巨噬细胞混合。有人提出，星形胶质细胞和小胶质细胞之间的这种接触逆转了铁蛋白生物合成和铁掺入的解偶联，并启动了铁的储存和含铁血黄素的形成。
The resolution of an intracerebral hemorrhage can be measured by the occurrence of hemosiderin. Extravasation of blood elicits a cellular reaction in the adjacent surviving tissue where the lesion activates resident microglia and attracts many more phagocytes from the blood stream. The signals for this migration into the perifocal reactive zone are not fully understood but it is likely that proteins in the coagulated blood contribute to cellular activation, Tn order to study the role of plasma proteins in the pathogenesis of the perifocal reactive zone, intracerebral injections of either autologous whole blood (0.1 ml) or an equal volume of washed autologous red blood cells (RBC) in lactated Ringer's solution were made in adult rabbits. The amount of total iron was the same (30 mu g). The cellular responses to the injections were studied by iron histochemistry and immunocytochemistry for ferritin, the ferritin repressor protein (FRP), the glial fibrillary acidic protein (GFAP), and the complement receptor CR3. Experimental hematomas resolved much more slowly after the injection of whole blood than after the injection of RBC. Qualitative microglial and astrocytic responses were quite similar. However, at 48 h, iron- and ferritin-reactive microglia were more numerous following the injection of whole blood. After injections of either type, ferritin-immunoreactive cells were more abundant than iron-positive cells. This observation implied that the biosynthesis of holoferritin protein and iron incorporation proceeded independently. Expression of CR3 on the surface of microglia was much more prominent after whole blood, suggesting a role of inactivated complement 3b in the attraction of additional phagocytes. Conversion to hemosiderin began at 5 days after the injection of either blood or RBC. The lesions caused initial destruction of astrocytes in the perifocal zone as judged by GFAP- and FRP-immunoreactivity. However, at 5 days, astrocytic processes reentered the perifocal zone and intermingled with microglia and macrophages. It is proposed that this contact between astrocytes and microglia reversed the uncoupling of ferritin biosynthesis and iron incorporation and initiated the storage of iron and formation of hemosiderin.