Nicotinamide Reduces the Infarct Volume in a Rat Model of Transient Middle Cerebral Artery Occlusion
Korean Journal of Pathology
;
: 93-102, 2006.
Article
in Korean
| WPRIM
| ID: wpr-210305
ABSTRACT
BACKGROUND:
Cerebral ischemia depletes ATP and causes irreversible tissue injury. Nicotinamide is a precursor of NAD+ and it is also a poly (ADP-ribose) polymerase (PARP) inhibitor that increases the neuronal ATP concentration and so protects against stroke. Therefore we examined whether nicotinamide could protect against cerebral ischemia by using a model of transient middle cerebral artery occlusion (MCAO) (reperfusion 2 h post ischemia) in Sprague-Dawley rats.METHODS:
Nicotinamide (500 mg/kg) or normal saline was administered intraperitoneally 24 and 0 h before and after MCAO, respectively. The infarction volumes were determined with triphenyltetrazolium chloride staining 24 h after reperfusion. The nitrotyrosine, PAR polymer and PARP-1 expressions were examined by immunohistochemistry with using brain slices obtained from the rats that were sacrificed at 0, 15, 30, 60 and 120 min after reperfusion.RESULTS:
The infarction volumes were significantly attenuated (21.8%, p<0.05). The nitrotyrosine expressions were increased at 0, 15 and 30 min, and those expressions for PARP polymer and PARP-1 were increased at 60 and 120 min, respectively. Nicotinamide partly reduced the expressions for nitrotyrosine and PAR polymer except for PARP-1.CONCLUSIONS:
These results suggest that nicotinamide may attenuate ischemic brain injury through its antioxidant activity and the inhibition of PARP-1.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Polymers
/
Brain
/
Brain Injuries
/
Immunohistochemistry
/
Reperfusion
/
Brain Ischemia
/
Adenosine Triphosphate
/
Rats, Sprague-Dawley
/
Niacinamide
/
Middle Cerebral Artery
Limits:
Animals
Language:
Korean
Journal:
Korean Journal of Pathology
Year:
2006
Type:
Article
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