Activation of endogenous gas molecules and its spinal cord protection by hydrogen sulfide
| Project/Area Number |
25293329
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Partial Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Anesthesiology
|
|---|
| Research Institution | University of the Ryukyus |
|---|
Principal Investigator |
KAKINOHANA MANABU 琉球大学, 医学(系)研究科(研究院), 教授 (20274897)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OSHIRO Masakatsu 琉球大学, 医学部附属病院, 助教 (00315483)
NAKAMURA Seiya 琉球大学, 大学院医学研究科, 准教授 (00363680)
NOGUCHI Nobuhiro 琉球大学, 医学部附属病院, 助教 (80457671)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2015: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
|
|---|
| Keywords | 遅発性脊髄障害 / 硫化水素 / 抗アポトーシス蛋白 / Bcl-XL / 抗炎症効果 / 硫化水素ガス / NFκB / アポトーシス / 脊髄神経細胞死 / 炎症性サイトカイン / HO-1 / 脊髄神経 / 神経変性 |
|---|
| Outline of Final Research Achievements |
The investigating the mechanism for neuroprotective effect by hydrogen sulfide (H2S) inhalation therapy after spinal cord ischemia in mice was done. H2S inhalation therapy started at 24 hours of spinal cord ischemia could provide significant neuroprotective effect compared to air inhalation (control). Some inflammatory cytokine (TNF-alph, IL-1beta, IL-6) increased significantly during onset of delayed paraplegia, which was completely blocked by H2S inhalation therapy. Of interesting, this effects could not be observed in inducible NOS (NOS2) deficient mice. H2S therapy could produce Bcl-XL, antiapoptotic protein, in the spinal cord and the primary neuronal culture cells. Based on these results, neuroprotective effects induced by H2S inhalation therapy may be associated with the synthesis of antiapoptotic protein as well as anti-inflammation, and NOS2 might be essential for its effects.
|
Report
(4 results)
Research Products
(5 results)
