Focal cerebral ischemia enhances glial expression of ecto-5'-nucleotidase
Focal cerebral ischemia enhances glial expression of ecto-5'-nucleotidase
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DOI：
10.1016/s0006-8993(97)00559-3
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发表时间：
1997-08-22
期刊：
影响因子：
2.9
通讯作者：
Zimmermann, H
中科院分区：
文献类型：
--
作者：
Braun, N;Lenz, C;Zimmermann, H
研究了永久性大脑中动脉闭塞（MCAO）后 6 小时以及 1、2 和 7 天时缺血对大鼠脑中 ecto-5'-核苷酸酶反应性表达的影响，使用组织学方法将梗死脑中 5'-核苷酸酶的分布与星形胶质细胞（胶质纤维酸性蛋白（GFAP））和小胶质细胞（补体受体 3 型，抗体 OX42）的标记物进行比较。染色或免疫组织化学。通过免疫组织化学，5'-核苷酸酶可以与反应性星形胶质细胞相关，通过酶组织化学，5'-核苷酸酶可以与反应性小胶质细胞相关。在未经处理的对照中，5'-核苷酸酶仅与海马和脑膜下间隙中的星形胶质细胞相关。缺血后，该酶在梗死区周围组织中的反应性星形胶质细胞上表达。 MCAO后6小时观察到单个反应性星形胶质细胞，并且星形胶质细胞的表达在接下来的几天内持续增强。 5'-核苷酸酶活性的酶组织化学分析显示，梗死组织周围的反应产物在缺血后增加。 MCAO 7 天后，梗塞区域的边缘出现一条不连续的反应产物带（0.2-0.4 毫米）。该 5'-核苷酸酶活性带与 OX42 的免疫反应性带共定位，表明表达 5'-核苷酸酶的小胶质细胞大量积累。我们的结果表明，永久性 MCAO 后的缺血会导致梗死区附近组织内核苷酸水解能力的上调。受损细胞释放的核苷酸可以被水解，最终形成的腺苷可以发挥神经保护功能，限制损伤程度。 (C) 1997 Elsevier Science B.V.
The effect of ischemia on the reactive expression of ecto-5'-nucleotidase in rat brain was studied 6 h and 1, 2 and 7 days after permanent middle cerebral artery occlusion (MCAO), The distribution of 5'-nucleotidase in the infarcted brain was compared to markers for astrocytes (glial fibrillary acidic protein (GFAP)) and microglia (complement receptor type 3, antibody OX42) using histological staining or immunohistochemistry. 5'-Nucleotidase could be associated with reactive astrocytes by immunohistochemistry and with reactive microglia by enzyme histochemistry. In the untreated control 5'-nucleotidase was associated with astrocytes only in the hippocampus and the submeningeal space. After ischemia the enzyme was expressed on reactive astrocytes in the tissue surrounding the volume of infarction. Individual reactive astrocytes were observed 6 h after MCAO and the astrocytic expression became continuously enhanced during the following days. An enzyme histochemical analysis of 5'-nucleotidase activity revealed a postischemic increase in reaction product around the infarcted tissue. Seven days after MCAO a discrete band (0.2-0.4 mm) of reaction product characterized the rim of the infarcted area. This band of activity of 5'-nucleotidase colocalized with a band of immunoreactivity for OX42, indicative of an intense accumulation of 5'-nucleotidase expressing microglia. Our results suggest that ischemia following permanent MCAO results in an upregulation of the capacity for the hydrolysis of nucleotides within the tissue adjacent to the infarcted volume. Nucleotides released from the damaged cells can be hydrolyzed and the adenosine eventually formed may exert neuroprotective functions limiting the extent of damage. (C) 1997 Elsevier Science B.V.