| Project/Area Number |
25560261
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | Kobe University |
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Principal Investigator |
Fujino hidemi 神戸大学, 保健学研究科, 教授 (20278998)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Akihiko 京都大学, 大学院人間・環境学研究科, 教授 (90184548)
KONDO Hiroyo 名古屋女子大学, 家政学部, 准教授 (50333183)
MURAKAMI Shinichiro 姫路獨協大学, 医療保健学部, 教授 (30454763)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | カヘキシー / 電気刺激 / 筋萎縮 |
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| Outline of Final Research Achievements |
The present study sought to evaluate the effect of electrical stimulation (ES) by using kilohertz frequency on muscle atrophy and oxidative metabolism impairment induced by cachexia. Cachexia induced increased plasma levels of inflammatory cytokines, significant muscle mass loss, decreased fiber cross-sectional area, and an up-regulation of atrogin-1 and ubiquitinated proteins in the skeletal muscle. In addition, Cachexia decreased succinate dehydrogenase (SDH) and citrate synthase (CS) activity, PGC-1α expression, and increased the phosphorylation of p38 MAPK. ES attenuated the sepsis-induced loss of muscle mass and decreased muscle fiber cross-sectional area, as well as attenuated the atrogin-1 and ubiquitinated protein up-regulation. ES also attenuated the changes in SDH and CS activities, p38 MAPK, and PGC-1ɑ. These results suggest that ES could prevent muscle atrophy and decrement in muscle oxidative metabolism induced by pro-inflammatory cytokines in cachexia.
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