| Project/Area Number |
24790258
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | Nagasaki University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
|---|
| Keywords | 血液脳関門 / 虚血再還流 / 高血糖 / トランスフォーミング増殖因子-β / シロスタゾール / ペリサイト / Neurovascular Unit / Neurovascular unit |
|---|
| Research Abstract |
The blood-brain barrier (BBB), a member of the neurovascular unit (NVU), functions in communication between brain capillary endothelium and other neighboring cells such as astrocytes and pericytes. BBB dysfunction plays a crucial role in brain edema formation and central nervous system disorders. Therefore, the experimental BBB dysfunction models under the pathological condition are applicable to search the protective agents against BBB dysfunction.
We have developed and characterized a new in vitro BBB model (BBB Kit) using primary cultures of the three main BBB-related cells obtained from rat brains. We attempted to make three types of BBB dysfunction models and succeeded in making following models: (i) hypoxia/reoxygenation model, (ii) hyperglycemia model, (iii) AGE-related ischemia model. We found that cilostazol protected the BBB against AGE-related ischemia, through an inhibitory mechanism on TGF-beta signaling.
|
