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

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  • KATSUKI Ryo
    Department of Lactic Acid Bacteria Technology Core Technology Laboratories, Asahi Quality & Innovations, Ltd.
  • SAKATA Shinji
    Department of Lactic Acid Bacteria Technology Core Technology Laboratories, Asahi Quality & Innovations, Ltd.
  • NAKAO Reiko
    Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
  • OISHI Katsutaka
    Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST) Department of Applied Biological Science, Graduate School of Science and Technology, Tokyo University of Science Department of Computational and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo School of Integrative and Global Majors (SIGMA), University of Tsukuba
  • NAKAMURA Yasunori
    Department of Lactic Acid Bacteria Technology Core Technology Laboratories, Asahi Quality & Innovations, Ltd.

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  • <i>Lactobacillus curvatus</i> CP2998 Prevents Dexamethasone-Induced Muscle Atrophy in C2C12 Myotubes

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<p>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.</p>

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