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创伤性脑损伤后胶质细胞中血红素加氧酶-1(HO-1)的诱导。

Induction of heme oxygenase-1 (HO-1) in glia after traumatic brain injury.

作者信息

Fukuda K, Richmon J D, Sato M, Sharp F R, Panter S S, Noble L J

机构信息

Department of Neurosurgery, University of California, San Francisco, USA.

出版信息

Brain Res. 1996 Oct 14;736(1-2):68-75. doi: 10.1016/0006-8993(96)00680-4.

DOI:10.1016/0006-8993(96)00680-4
PMID:8930310
Abstract

In this study we examined the induction of heme oxygenase-1 (HO-1) in glia in the traumatized rat brain. HO-1 was immunolocalized in fixed sections of brain 3 h to 5 days after injury. Induction of this enzyme in astrocytes, microglia/macrophages, and oligodendrocytes was evaluated using immunofluorescent double labeling with monoclonal antibodies to glial fibrillary acidic protein, complement C3bi receptor, and myelin basic protein. Induction of HO-1 was apparent in the injured hemisphere and cerebellum as early as 24 h postinjury. The protein was likewise noted in similar regions of the brain at 72 h postinjury but appeared to be more widespread in its distribution. At 5 days postinjury, there was a notable decline in the degree of immunostaining for HO-1. HO-1 was typically induced in astrocytes in the cerebral cortex at the site of impact, in the deep cortical layers adjacent to the hemorrhagic lesions, and in the hippocampus. HO-1 was induced in Bergmann glia in the vermis of cerebellum. In addition, HO-1 was also induced in microglia/macrophages scattered throughout the ipsilateral cerebral cortex, cerebellum and subarachnoid space. These findings demonstrate prolonged glial induction of HO-1 in the traumatized brain. Such a response may reflect a protective role of these cells against secondary insults including oxidative stress.

摘要

在本研究中,我们检测了创伤大鼠脑内胶质细胞中血红素加氧酶-1(HO-1)的诱导情况。在损伤后3小时至5天的脑固定切片中对HO-1进行免疫定位。使用针对胶质纤维酸性蛋白、补体C3bi受体和髓鞘碱性蛋白的单克隆抗体进行免疫荧光双标记,评估该酶在星形胶质细胞、小胶质细胞/巨噬细胞和少突胶质细胞中的诱导情况。HO-1的诱导在损伤后24小时即在损伤半球和小脑中明显可见。在损伤后72小时,该蛋白在脑的类似区域也有发现,但其分布似乎更广泛。在损伤后5天,HO-1的免疫染色程度显著下降。HO-1通常在撞击部位的大脑皮质星形胶质细胞、出血性病变相邻的深层皮质以及海马体中被诱导。HO-1在小脑蚓部的伯格曼胶质细胞中被诱导。此外,HO-1也在散在于同侧大脑皮质、小脑和蛛网膜下腔的小胶质细胞/巨噬细胞中被诱导。这些发现表明创伤脑内胶质细胞对HO-1的诱导持续存在。这种反应可能反映了这些细胞对包括氧化应激在内的继发性损伤的保护作用。

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