Project/Area Number |
15K19996
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Orthopaedic surgery
|
Research Institution | Kobe University |
Principal Investigator |
SAKATA Ryosuke 神戸大学, 医学研究科, 医学研究員 (50579323)
|
Research Collaborator |
MIFUNE Yutaka
INUI Atsuyuki
UEDA Yasuhiro
KATAOKA Takeshi
|
Project Period (FY) |
2015-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | アディポネクチン / 筋萎縮 / 脂肪変性 / 慢性疼痛 / 慢性炎症 / 神経断裂 / 腱断裂 / 脂肪浸潤 / アディポカイン |
Outline of Final Research Achievements |
Skeletal muscle atrophy with fatty degeneration and infiltration is often caused by tendon rupture or nerve damage. Adipokines secreted from infiltrated adipocyte is known to contribute to chronic inflammation. We focused on Adiponectin, and evaluated its effect on chronic inflammation. We added Adiponectin to the muscle-derived cells cultured under inflammatory circumstances. Adiponectin showed the anti-inflammatory effect in this experiment. In in vivo experiment, muscle atrophy and fatty infiltration were observed in both torn tendon group and nerve damage group. The inflammatory cytokine was stimulated in atrophied and degenerated muscle. Simultaneously, Adiponectin was down-regulated in the endmysium of the atrophied muscle. Our results suggest that, in the atrophied and fatty infiltrated muscle caused by trauma such as tendon rupture and nerve damage, inflammation delays and chronic adipose inflammation would aggravate the clinical outcome.
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