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Isobavachalcone attenuates myotube atrophy induced by TNF‐α through muscle atrophy F‐box signaling and the nuclear factor erythroid 2‐related factor 2 cascade
Author(s) -
Hur Jinyoung,
Kim Mina,
Choi Sang Yoon,
Jang YoungJin,
Ha Tae Youl
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6235
Subject(s) - atrophy , muscle atrophy , myogenin , skeletal muscle , myocyte , oxidative stress , tumor necrosis factor alpha , myopathy , myosin , endocrinology , medicine , biology , myogenesis , microbiology and biotechnology
Skeletal muscle atrophy is a condition characterized by damaged muscle fibers and reduced numbers of muscle cells due to various causes. Muscle atrophy is associated with chronic diseases, such as heart failure, diabetes, and aging‐related diseases. Isobavachalcone (IBC) is a flavonoid found in various foods and natural products, and studies have investigated its diverse effects, including its neuroprotective and anticancer effects. However, no studies have evaluated the effects of IBC on muscle atrophy. Thus, in this study, we assessed the effects of IBC on prevention of muscle atrophy. To evaluate the preventive effects of IBC on muscle atrophy, we used C2C12 myoblasts and induced muscle atrophy by tumor necrosis factor (TNF)‐α. IBC regulated the expression levels of muscle atrophy F‐box and muscle RING finger‐1 in response to damaged muscle cells, thereby restoring the expression of myosin heavy chain and myogenin. Moreover, IBC regulated the phosphorylation of the nuclear factor‐κB and p38 and upregulated the expression of nuclear factor erythroid 2‐related factor 2 and heme oxygenase‐1, which are involved in regulating oxidative stress. Our results indicated that IBC acted to relieve TNF‐α‐induced skeletal muscle atrophy by regulating the factors related to inflammation and oxidative stress.