| Project/Area Number |
14570585
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurology
|
|---|
| Research Institution | Shinshu University |
|---|
Principal Investigator |
KOH Shousei Shinshu University, School of Health Sciences, Professor, 医学部, 教授 (80143981)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Motoki Shinshu University, School of Health Sciences, Professor, 医学部, 教授 (60223088)
|
|---|
| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
|---|
| Keywords | multiple sclerosis (MS) / demyelinating disease / experimental autoimmune encephalomyelitis (EAE) / cyclooxygenase / lipoxygenase / prostaglandine / phenidone / リポカリン型プロスタグランジン(PG)D合成酵素(L-PGDS) / 造血器型プロスタグランジン(PG)D合成酵素(H-PGDS) / ミエリンオリゴデンドロサイト糖蛋白質(MOG) |
|---|
| Research Abstract |
We studied the effects of oral administration of phenidone on the expression of the pro-inflammatory mediators, nitric oxide synthase (iNOS) and cyclooxygenase-(COX-) 1,2,and 5-lipoxygenase (5-LOX) in rats with experimental autoimmune encephalomyelitis (EAE). Phenidone (200mg/kg) was administered orally for 13 days after the induction of EAE by immunization with guinea pig myelin basic protein and complete Freund's adjuvant. The onset (P<0.001) and severity (P<0.05) of EAE paralysis in phenidone treated animals were delayed and suppressed significantly compared with vehicle-treated controls. Western blot analysis showed that expression of COX-1, 2 and 5-LOX decreased significantly in the spinal cords of phenidone-treated rats compared with vehicle-treated controls (P<0.05) and this finding was paralleled by immunohistochemical observations. These results suggest that the amelioration by phenidone of paralysis in rats with EAE is mediated in part by the suppression of COX and 5-LOX.
|
