Glial Damage After Transient Focal Cerebral Ischemia in Rats
Glial Damage After Transient Focal Cerebral Ischemia in Rats
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DOI：
10.1007/s12031-008-9165-4
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发表时间：
2009-06-01
影响因子：
3.1
通讯作者：
Araki, Tsutomu
中科院分区：
文献类型：
--
作者：
Matsuda, Shunsuke;Umeda, Masahiro;Araki, Tsutomu
我们研究了大鼠大脑中动脉闭塞引起的局灶性脑缺血90分钟后1至15天纹状体中8-羟基-2 '-脱氧鸟苷（8-OHdG）免疫反应性（作为DNA损伤的标志物）和单链DNA（ssDNA）免疫反应性（作为细胞凋亡的标志物）的免疫组织化学变化。在本研究中，在局灶性脑缺血后3天，在同侧纹状体中观察到MAP 2免疫染色的显著丧失。局灶性脑缺血后1天和3天，在同侧纹状体中观察到ssDNA免疫反应性凋亡神经元的数量显著增加。与此相反，8-OHdG-免疫阳性细胞的密度显着增加，观察到在同侧纹状体从3至15天后局灶性脑缺血。我们的双标记免疫化学研究表明，8-OHdG免疫反应观察到的isolectin B-4阳性的小胶质细胞和胶质细胞酸性蛋白免疫阳性的星形胶质细胞在同侧纹状体局灶性脑缺血后7天。这些结果表明，局灶性脑缺血可导致同侧纹状体中的小胶质细胞和星形胶质细胞的数量显着增加，DNA氧化损伤。此外，我们的研究结果表明，大多数小胶质细胞和星形胶质细胞在同侧纹状体局灶性脑缺血后可能不会死亡的凋亡。因此，我们的研究结果提供了新的证据表明，局灶性脑缺血可导致大多数小胶质细胞和星形胶质细胞的DNA氧化损伤。
We investigated the immunohistochemical changes of 8-hydroxy-2'-deoxyguanosine (8-OHdG) immunoreactivity as a marker of DNA damage and single-strand DNA (ssDNA) immunoreactivity as a marker of apoptosis in the striatum from 1 up to 15 days after 90 min of focal cerebral ischemia caused by middle cerebral artery occlusion in rats. In the present study, marked loss of MAP2 immunostaining was observed in the ipsilateral striatum 3 days after focal cerebral ischemia. A significant increase in the number of ssDNA-immunoreactive apoptotic neurons was observed in the ipsilateral striatum 1 and 3 days after focal cerebral ischemia. In contrast, a significant increase in densities of 8-OHdG-immunopositive cells was observed in the ipsilateral striatum from 3 up to 15 days after focal cerebral ischemia. Our double-labeled immunochemical study showed that 8-OHdG immunoreactivity was observed in both isolectin B-4-positive microglia and glial fibrillary acidic protein-immunopositive astrocytes in the ipsilateral striatum 7 days after focal cerebral ischemia. These results suggest that focal cerebral ischemia can cause a marked increase in the number of microglia and astrocytes with oxidative DNA damage in the ipsilateral striatum. Furthermore, our results show that most microglia and astrocytes in the ipsilateral striatum after focal cerebral ischemia may not die by apoptosis. Thus, our findings provide novel evidence that focal cerebral ischemia can cause oxidative DNA damage in most microglia and astrocytes.