Pyropiayezoensis protein protects against TNF‑α‑induced myotube atrophy in C2C12 myotubes via the NF‑κB signaling pathway.

Abstract

The protein extracted from red algae Pyropia yezoensis has various biological activities, including anti-inflammatory, anticancer, antioxidant, and antiobesity properties. However, the effects of P. yezoensis protein (PYCP) on tumor necrosis factor-α (TNF-α)-induced muscle atrophy are unknown. Therefore, the present study investigated the protective effects and related mechanisms of PYCP against TNF-α-induced myotube atrophy in C2C12 myotubes. Treatment with TNF-α (20 ng/ml) for 48 h significantly reduced myotube viability and diameter and increased intracellular reactive oxygen species levels; these effects were significantly reversed in a dose-dependent manner following treatment with 25–100 µg/ml PYCP. PYCP inhibited the expression of TNF receptor-1 in TNF-α-induced myotubes. In addition, PYCP markedly downregulated the nuclear translocation of nuclear factor-κB (NF-κB) by inhibiting the phosphorylation of inhibitor of κB. Furthermore, PYCP treatment suppressed 20S proteasome activity, IL-6 production, and the expression of the E3 ubiquitin ligases, atrogin-1/muscle atrophy F-box and muscle RING-finger protein-1. Finally, PYCP treatment increased the protein expression levels of myoblast determination protein 1 and myogenin in TNF-α-induced myotubes. The present findings indicate that PYCP may protect against TNF-α-induced myotube atrophy by inhibiting the proinflammatory NF-κB pathway.