일시적 국소 뇌허혈손상에서 신경세포의 세포자멸사와 Inducible Nitric Oxide Synthase 발현

• Published in: Journal of pathology and translational medicine pp. 364 - 371
• Main Authors: 이병육, 황성규, 강구성, 전홍화, 이영미, 김정완, 곽은경, 박지영, 손윤경
• Format: Journal Article
• Language: Korean
• Published: 대한병리학회 01-12-2004
• Subjects: 병리학
• ISSN: 2383-7837; 2383-7845

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. KCI Citation Count: 0