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

被引:78
作者
Fukuda, K
Richmon, JD
Sato, M
Sharp, FR
Panter, SS
Noble, LJ
机构
[1] SAN FRANCISCO GEN HOSP,DEPT NEUROSURG,SAN FRANCISCO,CA 94110
[2] UNIV CALIF SAN FRANCISCO,DEPT NEUROSURG,SAN FRANCISCO,CA 94143
[3] UNIV CALIF SAN FRANCISCO,DEPT NEUROL,SAN FRANCISCO,CA 94143
[4] VET AFFAIRS MED CTR,SAN FRANCISCO,CA 94121
关键词
heme oxygenase; astrocyte; microglia; macrophage; Bergmann glia; heat shock protein;
D O I
10.1016/0006-8993(96)00680-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
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页码:68 / 75
页数:8
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