Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia
이병욱, 황성규, 박지영, 강구성, 김정완, 손윤경, Quan Hong-Hua, 이영미, 곽은경,
소속 상세정보
이병욱 ( Yi Byoung-Yuk )
마산삼성병원 병리과
황성규 ( Hwang Sung-Kyoo )
경북대학교 의과대학 신경외과학교실
박지영 ( Park Ji-Young )
성균관대학교 의과대학 삼성제일병원 병리과
강구성 ( Kang Ku-Seong )
경북대학교 의과대학 병리학교실
김정완 ( Kim Jung-Wan )
경북대학교 치과대학 구강미생물학교실
손윤경 ( Sohn Yoon-Kyung )
경북대학교 의과대학 병리학교실
( Quan Hong-Hua )
경북대학교 의과대학 병리학교실
이영미 ( Lee Young-Mi )
경북대학교 의과대학 병리학교실
곽은경 ( Kwak Eun-Kyoung )
경북대학교 치과대학 구강병리학교실
KMID : 0357920040380060364
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.
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.
키워드
Focal ischemia;Reperfusion;Brain;Apoptosis;Inducible nitric oxide synthase
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