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著者: Daisuke Yamamoto, Taiki Maki, Elizabeth Henny Herningtyas, Nobuko Ikeshita, Hiromi Shibahara, Yuka Sugiyama, Shiho Nakanishi, Keiji Iida, Genzo Iguchi, Yutaka Takahashi, Hidesuke Kaji, Kazuo Chihara, Yasuhiko Okimura
雑誌名: Muscle Nerve. 2010 Jun;41(6):819-27. doi: 10.1002/mus.21621.
Abstract/Text
We investigated the utility of branched-chain amino acids (BCAA) in dexamethasone-induced muscle atrophy. Dexamethasone (600 microg/kg, intraperitoneally) and/or BCAA (600 mg/kg, orally) were administered for 5 days in rats, and the effect of BCAA on dexamethasone-induced muscle atrophy was evaluated. Dexamethasone decreased total protein concentration of rat soleus muscles. Concomitant administration of BCAA reversed the decrease. Dexamethasone decreased mean cross-sectional area of soleus muscle fibers, which was reversed by BCAA. Dexamethasone increased atrogin-1 expression, which has been reported to play a pivotal role in muscle atrophy. The increased expression of atrogin-1 mRNA was significantly attenuated by BCAA. Furthermore, dexamethasone-induced conversion from microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II, which is an indicator of autophagy, was blocked by BCAA. These findings suggest that BCAA decreased protein breakdown to prevent muscle atrophy. BCAA administration appears to be useful for prevention of steroid myopathy.
PMID 20169591 Muscle Nerve. 2010 Jun;41(6):819-27. doi: 10.1002/mus.21621.
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