The Protective Effect of
Aminoguanidine on Cerebral Ischemic Damage in the Rat Brain
V. DANIELISOVÁ, M. NÉMETHOVÁ, J. BURDA
Department of Neurochemistry, Institute of Neurobiology, Slovak
Academy of Science, Košice. Slovak Republic
Received April 8, 2003
Accepted November 15, 2003
Summary
The NADPH-diaphorase (NADPH-d) histochemical technique is
commonly used to localize the nitric oxide (NO) produced by the
enzyme nitric oxide synthase (NOS) in neural tissue. The
expression of inducible nitric oxide synthase (iNOS) is induced
in the late stage of cerebral ischemia, and NO produced by iNOS
contributes to the delay in recovery from brain neuronal damage.
The present study was performed to investigate whether the
increase in nitric oxide production via inducible nitric oxide
synthase was suppressed by the administration of aminoguanidine,
a selective iNOS inhibitor, as it follows a decrease of
NADPH-diaphorase activity (a marker for NOS) after four-vessel
occlusion used as an ischemic model. The administration of
aminoguanidine (100 mg/kg i.p., twice per day up to 3 days
immediately after the ischemic insult) reduced the number of
NADPH-diaphorase positive cells to control levels. Our results
indicated that aminoguanidine suppressed NADPH-diaphorase
activity, and also decreased the number of NADPH-diaphorase
positive cells in the CA1 region of the hippocampus following
ischemic brain injury.
Key words
Cerebral ischemia • Hippocampus • NADPH-diaphorase • Nitric
oxide synthase • Aminoguanidine
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