Pyropia Yezoensis Peptide Protects Against Dexamethasone-Mediated Muscle Atrophy and Induces Myofiber Preservation
Presentation Number: SUN 252
Date of Presentation: April 2nd, 2017
Min-Kyeong Lee*1, Jeongwook Choi1, In-Hye Kim1, Youn-Hee Choi1 and Taek-Jeong Nam2
1Pukyong National University, Busan, Korea, Republic of (South), 2Pukyong Natl Univ, Busan, Korea, Republic of (South)
As we age, our ability to maintain muscle homeostasis is impaired, resulting in progressive decreases in muscle mass, strength, quality, and function. This phenomenon, termed “sarcopenia”, is associated with frailty, disability, impaired balance, and increased mortality. The present study investigated the protective effect of Pyropia yezoensis peptide (PYP1-5) against dexamethasone (DEX)-mediated muscle atrophy in C2C12 myotubes. Two major signaling pathways control skeletal muscle hypertrophy: the insulin-like growth factor-1/Akt signaling pathway increases skeletal muscle mass via the stimulation of protein synthesis and inhibition of protein degradation, while the myostatin signaling pathway negatively regulates skeletal muscle mass by reducing protein synthesis. To investigate the muscle hypertrophic effect of PYP1-5 on skeletal muscle cells, C2C12 myotubes were treated with 100 µM DEX and 500 ng/ml of PYP1-5 for 24 h. We confirmed the expression of muscle hypertrophy-related genes by Western blotting and real-time polymerase chain reaction. PYP1-5 increased the expression levels of phosphorylated IGF-IR and IRS-1 significantly. PYP1-5 also significantly increased the expression levels of phosphorylated PI3K, Akt, mTOR, and p70S6K. Furthermore, PYP1-5 inhibited DEX-induced atrophy by restoring myostatin signaling and FoxO3a. Taken together, our findings indicate that PYP1-5 may be a useful tool for protecting against muscle atrophy.
Nothing to Disclose: MKL, JC, IHK, YHC, TJN