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KMID : 0357920040380060364
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Korean Journal of Pathology
2004 Volume.38 No. 6 p.364 ~ p.371
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Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia
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Yi Byoung-Yuk
Hwang Sung-Kyoo
Park Ji-Young
Kang Ku-Seong
Kim Jung-Wan
Sohn Yoon-Kyung
Quan Hong-Hua
Lee Young-Mi
Kwak Eun-Kyoung
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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.
Conclusions: 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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KEYWORD
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Focal ischemia, Reperfusion, Brain, Apoptosis, Inducible nitric oxide synthase
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