The effect of
Sunphenon and Polyphenon 60 in oxidative stress response,
myogenic regulatory factors, inflammatory
cytokines, apoptotic and proteolytic pathways on H2O2-induced myotube
atrophy was addressed. Cellular responses of H2O2-induced C2C12 cells were examined, including
mRNA expression of
myogenic regulatory factors, such as MyoD and
myogenin, inflammatory pathways, such as TNF-α and
NF-kB, as well as
proteolytic enzymes, such as μ-
calpain and
m-calpain. The pre-treatment of
Sunphenon (50 μg/mL)/Polyphenon 60 (50 μg/mL) on H2O2-treated C2C12 cells significantly down-regulated the
mRNA expression of
myogenin and MyoD when compared to those treated with H2O2-induced alone. Additionally, the
mRNA expression of μ-
calpain and
m-calpain were significantly(p<0.05) increased in H2O2-treated C2C12 cells, whereas pre-treatment with
Sunphenon/Polyphenon significantly down-regulated the above genes, namely μ-
calpain and
m-calpain. Furthermore, the
mRNA expression of TNF-α and
NF-kB were significantly increased in H2O2-treated C2C12 cells, while pre-treatment with
Sunphenon (50 μg/mL)/Polyphenon 60 (50 μg/mL) significantly (p<0.05) down-regulated it when compared to the untreated control group.Subsequent analysis of
DNA degeneration and
caspase activation revealed that
Sunphenon (50 μg/mL)/Polyphenon 60 (50 μg/mL) inhibited activation of
caspase-3 and showed an inhibitory effect on
DNA degradation. From this result, we know that, in stress conditions, μ-
calpain may be involved in the
muscle atrophy through the suppression of
myogenin and MyoD. Moreover,
Sunphenon may regulate the skeletal muscle genes/promote skeletal muscle recovery by the up-regulation of
myogenin and MyoD and suppression of μ-
calpain and inflammatory pathways and may regulate the apoptosis pathways. Our findings suggest that dietary supplementation of
Sunphenon might reduce inflammatory events in muscle-associated diseases, such as myotube
atrophy.