Korean J Pathol.
2004 Dec;38(6):364-371.
Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia
- Affiliations
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- 1Departments of Pathology, Kyungpook National University, School of Medicine, Daegu, Korea. yksohn@knu.ac.kr
- 2Departments of Neurosurgery, Kyungpook National University, School of Medicine, Daegu, Korea.
- 3Departments of Oral Microbiology, College of Dentistry, Daegu, Korea.
- 4Departments of Oral pathology, College of Dentistry, Daegu, Korea.
- 5Department of Pathology, Masan Samsung Hospital, Masan, Koera.
- 6Department of Pathology, Samsung Cheil Hospital, School of Medicine, Sungkyunkwan University, Seoul, Korea.
Abstract
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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.
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