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.