| Project/Area Number |
18K17736
|
|---|
| Research Category |
Grant-in-Aid for Early-Career Scientists
|
| Allocation Type | Multi-year Fund |
|---|
| Review Section |
Basic Section 59010:Rehabilitation science-related
|
|---|
| Research Institution | Niigata University of Health and Welfare |
|---|
Principal Investigator |
Takahashi Hideaki 新潟医療福祉大学, リハビリテーション学部, 講師 (90636250)
|
|---|
| Project Period (FY) |
2018-04-01 – 2022-03-31
|
| Project Status |
Completed (Fiscal Year 2021)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 変形性膝関節症 / 力学的ストレス / TRPA1チャネル / 関節軟骨 / メカニカルストレス / メカノセンシング |
|---|
| Outline of Final Research Achievements |
We examined whether TRPA1 channels and oxidative stress are mutually involved in the development of osteoarthritis knee (OA: Osteoarthritis Knee) using a OA rat model. The results showed that OA severity scores were significantly lower in the TRPA1 channel selective inhibitor group in the femur and tibia, however, it did not completely prevent OA. In addition, we compared urinary markers of oxidative stress. The results showed a dose-dependent decrease in oxidative stress, however, there was no correlation with the expression of type II collagen.
|
| Academic Significance and Societal Importance of the Research Achievements |
変形性膝関節症は、難治性の退行変性疾患であり、一度変性した軟骨組織の修復は困難である。その理由の一つとして、軟骨変性に至る機序が複数要因かつ複数経路あることが指摘されている。今回、われわれは、力学的過負荷により軟骨変性に至る経路の解明に取り組んだ。軟骨変性に至る経路の一端を明らかにすることは、今後のリハビリテーション分野のみならず医学全般に大きく貢献するものである。
|
