FK506 abrogates delayed neuronal death via suppression of nitric oxide production in rats.

Autor: Sasaki T; Department of Neurology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan. tsasaki@sc.itc.keio.ac.jp, Hamada J, Shibata M, Gotoh J, Araki N, Fukuuchi Y
Jazyk: angličtina
Zdroj: Brain research [Brain Res] 2004 May 29; Vol. 1009 (1-2), pp. 34-9.
DOI: 10.1016/j.brainres.2004.01.088
Abstrakt: 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 NO(2)(-) 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 NO(2)(-) level significantly increased during ischemia. In the FK506 treatment group, there was no significant change in the NO(2)(-) 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.
Databáze: MEDLINE
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