Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia
Korean Journal of Pathology
;
: 364-371, 2004.
Article
in English
| WPRIM
| ID: wpr-112683
ABSTRACT
BACKGROUND:
Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis.METHODS:
We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups.RESULTS:
TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased.CONCLUSION:
These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Oxygen
/
Brain
/
RNA, Messenger
/
Reperfusion
/
Brain Ischemia
/
Ischemic Attack, Transient
/
Rats, Sprague-Dawley
/
Apoptosis
/
In Situ Nick-End Labeling
/
Infarction, Middle Cerebral Artery
Language:
English
Journal:
Korean Journal of Pathology
Year:
2004
Type:
Article
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