Abstract
Background and purpose: The mechanism of the neuroprotective effect of FK506 in relation to nitric oxide (NO) production has not been clarified in vivo. We have investigated the effect of FK506 on ischemia-induced NO production in association with the pathogenesis of delayed neuronal death (DND) in rats. Methods: In vivo microdialysis was performed in the hippocampus of male Sprague-Dawley rats (250-350 g). Dialysate samples were collected every 3 min. In the ischemia group (n=16), global ischemia was induced for 21 min and reperfusion was achieved. In the FK506 treatment group (n=25), FK506 (1 mg/kg, i.v.) was administered 21 min prior to the onset of global ischemia. Sham operations were done (n=15). The levels of NO2- in the dialysate samples were determined by the Griess reaction. The animals were decapitated 7 days after ischemia. Coronal brain sections were stained with hematoxylin and eosin. Results: In the ischemia group, the NO2 - level significantly increased during ischemia. In the FK506 treatment group, there was no significant change in the NO2 - level during ischemia. In histological examinations, FK506 treatment showed a neuroprotective effect against DND. Conclusions: The effect of FK506 inhibiting NO production contributes to the neuro-protective effect of FK506 on DND in the hippocampus.
Original language | English |
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Pages (from-to) | 34-39 |
Number of pages | 6 |
Journal | Brain Research |
Volume | 1009 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 2004 May 29 |
Externally published | Yes |
Keywords
- Cerebral ischemia
- Disorders of the nervous system
- Global
- Hippocampus
- Ischemia
- Microdialysis
- Nitric oxide
- Rat
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology