| Project/Area Number |
24700541
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Rehabilitation science/Welfare engineering
|
|---|
| Research Institution | Sapporo Medical University |
|---|
Principal Investigator |
YAMADA Takashi 札幌医科大学, 保健医療学部, 講師 (50583176)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 関節リウマチ / 筋力低下 / 炎症性サイトカイン / パーオキシナイトライト / 熱刺激 / 熱ショックタンパク質 / 筋弱化 / 固有張力 / 酸化ストレス / ミオシンATPase / SERCA |
|---|
| Research Abstract |
Patients with rheumatoid arthritis (RA) have significant muscle weakness, which has a major impact on disability in conjugation with disease activity. In the present study, we investigated the underlying mechanisms of contractile dysfunctions in skeletal muscle from adjuvant-induced arthritis (AIA) rats, which is a widely used animal model for RA. The results show intrinsic contractile dysfunction in extensor digitorum longus (EDL) muscles of AIA rats, which can be explained by the oxidative stress due to TNF-induced peroxynitrite overproduction. Moreover, take these findings and the antioxidative role of heat shock protein (Hsp) 72 into account, we investigated the effects of heat stress on the contractile properties and redox states of AIA EDL muscles. Our results show that heat stress markedly increases Hsp72 expression, but fails to ameliorate contractile dysfunctions and redox modifications in AIA EDL muscles.
|
