Abstract

The senescence-accelerated mouse strain P6 (SAMP6) was applied to investigate the effect of treatment with peptides from Antarctic Krill (AKP) on senile osteoporosis in vivo. Results showed that AKP significantly increased bone mineral density, improved bone biomechanical properties, and ameliorated trabecular bone microstructure by promoting bone anabolism in SAMP6. Neonatal murine calvaria culture system further demonstrated that AKP stimulated osteoblast-induced new osteoid and bone formation ex vivo. The mechanism revealed that AKP induced the secretion and expression of bone morphogenetic protein 2 (BMP2), which was identified as a potent osteoinductive factor, and activated BMP2-dependent Smads signaling by phosphorylation of Smad1. Wnt signaling shares the same osteogenesis related transcriptional factor Runx2 with BMP2/Smads pathway. AKP also induced the activation of Wnt/β-catenin signaling by upregulating the expression of Wnt10b and β-catenin. In conclusion, AKP ameliorated senile osteoporosis by activating BMP2/Smads and Wnt/β-catenin molecular pathways, thereby promoting bone formation. Practical applications As a novel food material, Antarctic krill possesses an enormous biomass and utilization potential. It contains the largest amount of protein among all recorded organisms worldwide and the protein biological value is better than other animal proteins. This study demonstrated that peptides hydrolyzed from Antarctic Krill exhibit antiosteoporotic activity, which may provide some theoretical basis for the high-value of Antarctic Krill protein as antiosteoporotic functional foods in future.

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