Effects of Indomethacin on Ischemia-induced Brain Injury.
- Author:
Doo Yeoul JUNG
1
;
Sun Yong BAEK
;
Min Kyoung CHO
;
Myoung Eun HAN
;
Bong Seon KIM
;
Jae Bong KIM
;
Sae Ock OH
Author Information
1. Department of Anatomy, School of Medicine, Pusan National University, Pusan, Korea.
- Publication Type:Original Article
- Keywords:
Cerebral ischemia;
Inflammation;
Neurogenesis;
Angiogenesis;
Gliosis
- MeSH:
Brain Injuries*;
Brain Ischemia;
Brain*;
Gliosis;
Indomethacin*;
Infarction;
Inflammation;
Ischemia;
Models, Animal;
Neurogenesis;
Quality of Life
- From:Korean Journal of Anatomy
2007;40(3):179-191
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cerebral ischemia can have severe results and disrupt quality of life. Current medicine is not effective at overcoming these problems. To find out more effective therapies, it is necessary to understand the microenvironment of cerebral injury after the ischemia. In the present study, to investigate the effects of inflammatory reaction, indomethacin, an anti-inflammatory drug, was used in a photothrombotic focal infarction rat model. It was revealed that cerebral ischemia increased neurogenesis in the subventricular (SVZ) and subgranular zones (SGZ), and in the penumbral region. Indomethacin treatment reduced the cerebral ischemia-induced neurogenesis by 86.2%, 53.8%, and 52.8% respectively. Cerebral ischemia increased gliosis and angiogenesis in the penumbral region and indomethacin reduced gliosis and angiogenesis by 48.2% and 58.1%, respectively. These results suggest that indomethacin treatment after the cerebral ischemia can reduce neurogenesis, angiogenesis, and gliosis in the penumbral region.
