Neuroprotective effect of FK506, an immunosuppressant, on transient global ischemia in gerbil

Delayed neuronal death (DND) in CA1 region after transient global ischemia is a well-known phenomenon, but its mechanism has not been clarified. In order to examine the involvement of nitric oxide (NO in DND, 7-nitro indazole (7NI), a selective neuronal NO synthase (nNOS inhibitor, and FK506, an imm...

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Veröffentlicht in:	Neuroscience letters 1996-03, Vol.206 (2), p.81-84
Hauptverfasser:	Tokime, Tomoo, Nozaki, Kazuhiko, Kikuchi, Haruhiko
Format:	Artikel
Sprache:	eng
Schlagworte:	7-Nitro indazole Animals Biological and medical sciences Cell Death - drug effects Delayed neuronal death Enzyme Inhibitors - therapeutic use FK506 Gerbil Gerbillinae Global ischemia Immunosuppressive Agents - therapeutic use Indazoles - therapeutic use Ischemic Attack, Transient - prevention & control Male Medical sciences Meriones unguiculatus Neurons - drug effects Neurons - pathology Neuropharmacology Neuroprotective agent Neuroprotective Agents - therapeutic use Nitric oxide Nitric Oxide - physiology Nitric Oxide Synthase - antagonists & inhibitors Pharmacology. Drug treatments Prosencephalon - blood supply Tacrolimus - therapeutic use
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Zusammenfassung:	Delayed neuronal death (DND) in CA1 region after transient global ischemia is a well-known phenomenon, but its mechanism has not been clarified. In order to examine the involvement of nitric oxide (NO in DND, 7-nitro indazole (7NI), a selective neuronal NO synthase (nNOS inhibitor, and FK506, an immunosuppressant which also inhibits nNOS, were administered intraperitoneally during and after transient global ischemia in gerbil. FK506 moderately ameliorated DND in a dose-dependent manner. However, 7NI showed only minor neuroprotective effects. These results show that DND is not mainly mediated by NO production via nNOS, and FK506 acts as a neuroprotective agent via unknown pathways other than nNOS inhibition.
ISSN:	0304-3940 1872-7972
DOI:	10.1016/S0304-3940(96)12438-1