Phosphorylated Peptides from Antarctic Krill (Euphausia superba) Prevent Estrogen Deficiency Induced Osteoporosis by Inhibiting Bone Resorption in Ovariectomized Rats

In the current study, we investigated the improvement of phosphorylated peptides from Antarctic krill Euphausia superba (PP-AKP) on osteoporosis in ovariectomized rats. PP-AKP was supplemented to ovariectomized Sprague–Dawley rats for 90 days. The results showed that PP-AKP treatment remarkably prev...

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Veröffentlicht in:Journal of agricultural and food chemistry 2015-11, Vol.63 (43), p.9550-9557
Hauptverfasser: Xia, Guanghua, Zhao, Yanlei, Yu, Zhe, Tian, Yingying, Wang, Yiming, Wang, Shanshan, Wang, Jingfeng, Xue, Changhu
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Sprache:eng
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Zusammenfassung:In the current study, we investigated the improvement of phosphorylated peptides from Antarctic krill Euphausia superba (PP-AKP) on osteoporosis in ovariectomized rats. PP-AKP was supplemented to ovariectomized Sprague–Dawley rats for 90 days. The results showed that PP-AKP treatment remarkably prevented the reduction of bone mass and improved cancellous bone structure and biochemical properties. PP-AKP also significantly decreased serum contents of tartrate-resistant acid phosphatase (TRACP), cathepsin K (Cath-k), matrix metalloproteinases-9 (MMP-9), deoxypyridinoline (DPD), C-terminal telopeptide of collagen I (CTX-1), Ca, and P. Mechanism investigation revealed that PP-AKP significantly increased the osteoprotegerin (OPG)/receptor activator of nuclear factor κB ligand (RANKL) ratio in mRNA expression, protein expression, and serum content. Further research suggested that NF-κB signaling pathways were inhibited by suppressing the mRNA and protein expressions of nuclear factor of activated T-cells (NFATc1) and tumor necrosis factor receptor-associated factor 6 (TRAF6), diminishing the mRNA expression and phosphorylation of nuclear factor κB p65 (NF-κB p65), three key transcription factors in NF-κB pathways. These results suggest that PP-AKP can improve osteoporosis by inhibiting bone resorption via suppressing the activation of osteoclastogenesis related NF-κB pathways.
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.5b04263