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 |
|---|---|
| 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 |
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Keywords
- Cerebral ischemia
- Disorders of the nervous system
- Global
- Hippocampus
- Ischemia
- Microdialysis
- Nitric oxide
- Rat
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
FK506 abrogates delayed neuronal death via suppression of nitric oxide production in rats. / Sasaki, Takahiro; Hamada, Junichi; Shibata, Mamoru; Gotoh, Jun; Araki, Nobuo; Fukuuchi, Yasuo.
In: Brain Research, Vol. 1009, No. 1-2, 29.05.2004, p. 34-39.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - FK506 abrogates delayed neuronal death via suppression of nitric oxide production in rats
AU - Sasaki, Takahiro
AU - Hamada, Junichi
AU - Shibata, Mamoru
AU - Gotoh, Jun
AU - Araki, Nobuo
AU - Fukuuchi, Yasuo
PY - 2004/5/29
Y1 - 2004/5/29
N2 - 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.
AB - 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.
KW - Cerebral ischemia
KW - Disorders of the nervous system
KW - Global
KW - Hippocampus
KW - Ischemia
KW - Microdialysis
KW - Nitric oxide
KW - Rat
UR - http://www.scopus.com/inward/record.url?scp=2142715917&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2142715917&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2004.01.088
DO - 10.1016/j.brainres.2004.01.088
M3 - Article
C2 - 15120581
AN - SCOPUS:2142715917
VL - 1009
SP - 34
EP - 39
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -