In this study, the effects of phosphorylated peptides from Antarctic krill (PP-AKP) on osteoporosis induced by dexamethasone were investigated in vivo. Results showed that PP-AKP significantly improved bone turnover status, reduced bone loss and degeneration of microarchitecture, in addition to accelerated bone formation. Further mechanism investigation revealed that PP-AKP suppressed the mRNA expression of MKP-1 and CB1, which activated the downstream osteogenesis-related MAPKs and PI3K/AKT/GSK-3β signaling pathways through elevation of the expression of the key factors p38, ERK, PI3K, AKT and β-catenin, in addition to osteogenic nuclear transcription factors Runx2 and OSX. Additionally, reduction in number of adipocytes and an increase in trabeculae in the bone marrow cavity, in addition to a decrease in abdominal adipose further verified that PP-AKP augmented bone formation with a comparable reduction in the accumulation of fat. In conclusion, PP-AKP ameliorated osteoporosis via promoting MAPKs and PI3K/AKT/GSK-3β pathways related to bone formation in dexamethasone-treated mice.

在这项研究中，在体内研究了南极磷虾（PP-AKP）磷酸化肽对地塞米松诱导的骨质疏松的影响。结果表明，PP-AKP可以显着改善骨骼更新状态，减少骨骼流失和微结构退化，此外还可以加速骨骼形成。进一步的机制研究表明，PP-AKP抑制了MKP-1和CB1的mRNA表达，从而通过提高关键因子p38，ERK， PI3K，AKT和β-连环蛋白，以及成骨核转录因子Runx2和OSX。此外，除腹部脂肪减少之外，骨髓腔中脂肪细胞数量的减少和小梁的增加进一步证实了PP-AKP可以增加骨骼的形成，并具有类似的脂肪积聚减少。综上所述，