Katsuki Ryo, Sakata Shinji, Nakao Reiko, Oishi Katsutaka, Nakamura Yasunori
Department of Lactic Acid Bacteria Technology Core Technology Laboratories, Asahi Quality & Innovations, Ltd.
Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST).
J Nutr Sci Vitaminol (Tokyo). 2019;65(5):455-458. doi: 10.3177/jnsv.65.455.
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.
为了研究热灭活的卷曲乳杆菌CP2998（CP2998）是否能抑制与泛素-蛋白酶体系统相关的糖皮质激素诱导的肌管萎缩，在有或没有CP2998存在的情况下，用 dexamethasone（DEX）处理小鼠骨骼肌C2C12肌管。DEX暴露显著降低了肌管直径，并增加了E3泛素连接酶MuRF1和MAFbx的mRNA表达水平。CP2998处理恢复了肌管直径，并剂量依赖性地降低了这些E3泛素连接酶的mRNA表达水平。CP2998处理还抑制了DEX诱导的糖皮质激素依赖性转录。我们的结果表明，CP2998通过抑制糖皮质激素受体激活来预防DEX诱导的肌肉萎缩。
