Correlation Between Neuronal Apoptosis and Expression of Inducible Nitric Oxide Synthase after Transient Focal Cerebral Ischemia.
- Author:
Byoung Yuk YI
1
;
Sung Kyoo HWANG
;
Ku Seong KANG
;
Hong Hua QUAN
;
Young Mi LEE
;
Jung Wan KIM
;
Eun Kyoung KWAK
;
Ji Young PARK
;
Yoon Kyung SOHN
Author Information
1. Departments of Pathology, Kyungpook National University, School of Medicine, Daegu, Korea. yksohn@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Focal ischemia;
Reperfusion;
Brain;
Apoptosis;
Inducible nitric oxide synthase
- MeSH:
Apoptosis*;
Brain;
Brain Ischemia*;
In Situ Nick-End Labeling;
Infarction, Middle Cerebral Artery;
Ischemia;
Ischemic Attack, Transient;
Necrosis;
Neurons*;
Nitric Oxide;
Nitric Oxide Synthase Type II*;
Oxygen;
Rats, Sprague-Dawley;
Reperfusion;
RNA, Messenger
- From:Korean Journal of Pathology
2004;38(6):364-371
- CountryRepublic of Korea
- Language:English
-
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.
