The Protective Effect of Aminoguanidine on Cerebral Ischemic Damage in the Rat Brain

Title:

The Protective Effect of Aminoguanidine on Cerebral Ischemic Damage in the Rat Brain

Creator:

Danielisová, V., Némethová, M., and Burda, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a0b76316-b713-4014-8490-118660f651a5
uuid:a0b76316-b713-4014-8490-118660f651a5

Subject:

Cerebral ischemia, Hippocampus, NADPH-diaphorase, Nitric oxide synthase, and Aminoguanidine

Type:

article, model:article, and TEXT

Description:

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.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2004 Volume:53 | Number:5

Harvested from:

CDK

Metadata only:

false