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Antioxidant effect of human placenta hydrolysate against oxidative stress on muscle atrophy

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Journal of Cellular Physiology

Published online on


--- - |2- Human placental hydrolysate required for the regulation of oxidative stress through the control of Mstn expression by nuclear factor‐κB, mitochondrial quality control, and autophagy process, leading to improved muscle atrophy. Sarcopenia, which refers to the muscle loss that accompanies aging, is a complex neuromuscular disorder with a clinically high prevalence and mortality. Despite many efforts to protect against muscle weakness and muscle atrophy, the incidence of sarcopenia and its related permanent disabilities continue to increase. In this study, we found that treatment with human placental hydrolysate (hPH) significantly increased the viability (approximately 15%) of H2O2‐stimulated C2C12 cells. Additionally, while H2O2‐stimulated cells showed irregular morphology, hPH treatment restored their morphology to that of cells cultured under normal conditions. We further showed that hPH treatment effectively inhibited H2O2‐induced cell death. Reactive oxygen species (ROS) generation and Mstn expression induced by oxidative stress are closely associated with muscular dysfunction followed by atrophy. Exposure of C2C12 cells to H2O2 induced abundant production of intracellular ROS, mitochondrial superoxide, and mitochondrial dysfunction as well as myostatin expression via nuclear factor‐κB (NF‐κB) signaling; these effects were attenuated by hPH. Additionally, hPH decreased mitochondria fission–related gene expression (Drp1 and BNIP3) and increased mitochondria biogenesis via the Sirt1/AMPK/PGC‐1α pathway and autophagy regulation. In vivo studies revealed that hPH‐mediated prevention of atrophy was achieved predominantly through regulation of myostatin and PGC‐1α expression and autophagy. Taken together, our findings indicate that hPH is potentially protective against muscle atrophy and oxidative cell death. - 'Journal of Cellular Physiology, Volume 234, Issue 2, Page 1643-1658, February 2019. '