Lactobacillus curvatus CP2998 Prevents Dexamethasone-Induced Muscle Atrophy in C2C12 Myotubes

被引:11
|
作者
Katsuki, Ryo [1 ]
Sakata, Shinji [1 ]
Nakao, Reiko [2 ]
Oishi, Katsutaka [2 ,3 ,4 ,5 ]
Nakamura, Yasunori [1 ]
机构
[1] Asahi Qual & Innovat Ltd, Dept Lact Acid Bacteria Technol Core Technol Labs, Moriya, Ibaraki 3020106, Japan
[2] Natl Inst Adv Ind Sci & Technol, Biomed Res Inst, Biol Clock Res Grp, Tsukuba, Ibaraki 3058566, Japan
[3] Tokyo Univ Sci, Dept Appl Biol Sci, Grad Sch Sci & Technol, Noda, Chiba 2788510, Japan
[4] Univ Tokyo, Grad Sch Frontier Sci, Dept Computat & Med Sci, Kashiwa, Chiba 2770882, Japan
[5] Univ Tsukuba, Sch Integrat & Global Majors SIGMA, Tsukuba, Ibaraki 3058577, Japan
关键词
lactic acid bacteria; sarcopenia; skeletal muscle; glucocorticoid; FoxO; KLF15; MuRF1; MAFbx; ubiquitin ligases; GLUCOCORTICOID-RECEPTOR; UBIQUITIN LIGASES; MURF1; MICROBIOTA; ATROGIN-1; AXIS;
D O I
10.3177/jnsv.65.455
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
To investigate whether heat-killed Lactobacillus curvatus CP2998 (CP2998) inhibits glucocorticoid-induced myotube atrophy which is associated with the ubiquitin-proteasome system, mouse skeletal muscle C2C12 myotubes were treated with dexamethasone (DEX) in the presence or absence of CP2998. DEX exposure significantly decreased myotube diameters and increased mRNA expression levels of MuRF1 and MAFbx, E3 ubiquitin ligases. CP2998 treatment restored myotube diameters and dose dependently decreased mRNA expression levels of these E3 ubiquitin ligases. CP2998 treatment also inhibited DEX-induced glucocorticoid dependent transcription. Our results suggest that CP2998 prevents DEX-induced muscle atrophy by suppressing glucocorticoid receptor activation.
引用
收藏
页码:455 / 458
页数:4
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