Abstract
Skeletal muscle atrophy has significant negative functional effects, especially on patients with inflammatory diseases. Tumor necrosis factor alpha (TNF-α) plays a crucial role in muscle pathology associated with muscle wasting and impairment of differentiation. The present study evaluated the anti-atrophic activity and related mechanism of a novel peptide (Tryptophan-Tyrosine-Lysine) derived from Olive Flounder surimi (OFSP), against TNF-α induced muscle atrophy in C2C12 myotubes. Molecular docking results showed that OFSP binds to TNF-α, inhibiting its binding to TNFR1 receptor. OFSP treatment increased the cell viability and decreased intracellular reactive oxygen species production caused by TNF-α. OFSP markedly downregulated the NF- κB pathway proteins phosphorylation, thereby inhibiting pathway activation. Furthermore, OFSP suppressed IL-6 production and expression of E2 ubiquitin ligases, atrogin-1/MAFbx and MuRF1, while increasing myogenic marker expressions. Current findings indicate that OFSP exhibits excellent anti-atrophic activity against inflammation-induced muscle atrophy, and these characteristics may be valuable in anti-atrophic functional food development.
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