1995 Fiscal Year Final Research Report Summary
Expression of Mn-SOD gene in the neonatal rat with hypoxic-ischemic brain damage.
| Project/Area Number |
06671168
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kobe University. School of Medicine, Department of Pediatrics |
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Principal Investigator |
TAKADA Satoshi Kobe University. School of Medicine, Department of Pediatrics, Assistant Professor, 医学部, 助手 (10216658)
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| Co-Investigator(Kenkyū-buntansha) |
UETANI Yoshiyuki Kobe University. School of Medicine, Department of Pediatrics, Associate Profess, 医学部, 講師 (40168620)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Mn-Superoxide dismutase / Hypoxic-ischemic encephalopathy / Dexamethasone / Immuno-peroxidase staining / Northern Blotting |
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| Research Abstract |
1. Expression of Mn-SOD gene in the developing rat brain.
Expression of Mn-SOD mRNA was studied in the developing rat brain by using Northern blotting analysis. Mn-SOD mRNA was observed in the fetal rat brain on gestational day 18, and its level increased during early neonatal days. Immuno-histochemical staining revealed that Mn-SOD positive cells were rich in CA3 area in the hippocampus in these days.
2. Effect of hypoxic-ischemic brain damage on the expression of Mn-SOD.
Ischemic changes were most evident in the cortex, hippocampus, striatum and thalamus. The infiltration of Mn-SOD positive astrocytes was observed in the regions surrounding these involved areas.
3. Effect of dexamethasone on the expression of Mn-SOD.
The treatment with dexamethasone suppressed the expression of Mn-SOD in the developing rat brain. In the rats treated with dexamethasone, both the number of GFAP positive cells and the number of the cortical cells in the cerebral cortex were less than those in the control rats. The administration of the dexamethasone also weakened the intensity of MBP immunostaining. Pretreatment with dexamethasone protected the developing brain from hypoxic-ischemic injury, and the infiltration of Mn-SOD positive astrocytes decreased in our experiment. These results suggest that the protection by dexamethasone was due to the suppression of the glial and neuronal cell maturation.
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