Postischemic Alterations of BDNF,NGF, HSP 70 and Ubiquitin Immunoreactivity in the Gerbil Hippocampus: Pharmacological Approach |
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Authors: | Toshiki Himeda Hiroko Tounai Natsumi Hayakawa Tsutomu Araki |
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Institution: | (1) Department of Drug Metabolism and Therapeutics, Graduate school and Faculty of Pharmaceutical Sciences, The University of Tokushima, 1-78 Sho-machi, Tokushima 770-8505, Japan |
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Abstract: | 1. We investigated the immunohistochemical alterations of BDNF, NGF, HSP 70 and ubiquitin in the hippocampus 1 h to 14 days
after transient cerebral ischemia in gerbils. We also examined the effect of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase inhibitor pitavastatin against the changes of BDNF, NGF, HSP 70 and ubiquitin in the hippocampus after cerebral
ischemia in the hippocampus after ischemia.
2. The transient cerebral ischemia was carried out by clamping the carotid arteries with aneurismal clips for 5 min.
3. In the present study, the alteration of HSP 70 and ubiquitin immunoreactivity in the hippocampal CA1 sector was more pronounced
than that of BDNF and NGF immunoreactivity after transient cerebral ischemia. In double-labeled immunostainings, BDNF, NGF
and ubiquitin immunostaining was observed both in GFAP-positive astrocytes and MRF-1-positive microglia in the hippocampal
CA1 sector after ischemia. Furthermore, prophylactic treatment with pitavastatin prevented the damage of neurons with neurotrophic
factor and stress proteins in the hippocampal CA1 sector after ischemia.
4. These findings suggest that the expression of stress protein including HSP 70 and ubiquitin may play a key role in the
protection against the hippocampal CA1 neuronal damage after transient cerebral ischemia in comparison with the expression
of neurotrophic factor such as BDNF and NGF. The present findings also suggest that the glial BDNF, NGF and ubiquitin may
play some role for helping surviving neurons after ischemia. Furthermore, our present study indicates that prophylactic treatment
with pitavastatin can prevent the damage of neurons with neurotrophic factor and stress proteins in the hippocampal CA1 sector
after transient cerebral ischemia. Thus our study provides further valuable information for the pathogenesis after transient
cerebral ischemia.
The first two authors contributed equally |
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Keywords: | cerebral ischemia neurotrophic factor stress protein gerbil 3-Hydroxy-3-methylglutaryl-coenzyme a reductase inhibitor |
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