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 s
ections of brain 3 h to 5 days after injury. Induction of this enzyme
in astrocytes, microglia/macrophages, and oligodendrocytes was evaluat
ed using immunofluorescent double labeling with monoclonal antibodies
to glial fibrillary acidic protein, complement C3bi receptor, and myel
in basic protein. Induction of HO-1 was apparent in the injured hemisp
here and cerebellum as early as 24 h postinjury. The protein was likew
ise noted in similar regions of the brain at 72 h postinjury but appea
red to be more widespread in its distribution. At 5 days postinjury, t
here was a notable decline in the degree of immunostaining for HO-1. H
O-1 was typically induced in astrocytes in the cerebral cortex at the
site of impact, in the deep cortical layers adjacent to the hemorrhagi
c lesions, and in the hippocampus. HO-1 was induced in Bergmann glia i
n the vermis of cerebellum. In addition, HO-1 was also induced in micr
oglia/macrophages scattered throughout the ipsilateral cerebral cortex
, cerebellum and subarachnoid space. These findings demonstrate prolon
ged 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.