Inhibitory effects of Atlantic cod () peptides on RANKL-induced osteoclastogenesis and osteoporosis in ovariectomized mice
Atlantic cod ( Gadus morhua ) is one of the most important fishes in the world with high nutritional value and economic value. However, the impact and underlying mechanism of the G. morhua peptides (GMPs) on osteoclastogenesis and bone mineral density (BMD) regulation remain unclear. The purpose of...
Saved in:
Published in | Food & function Vol. 13; no. 4; pp. 1975 - 1988 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Published |
21.02.2022
|
Online Access | Get full text |
Cover
Loading…
Summary: | Atlantic cod (
Gadus morhua
) is one of the most important fishes in the world with high nutritional value and economic value. However, the impact and underlying mechanism of the
G. morhua
peptides (GMPs) on osteoclastogenesis and bone mineral density (BMD) regulation remain unclear. The purpose of this study was to investigate the effects of GMPs on osteoclast formation and anti-osteoporosis activity
in vitro
and
in vivo
. The results showed that GMPs significantly reduced receptor activator of nuclear factor (RANKL) induced tartrate-resistant acid phosphatase (TRAP) activity, and decreased the expression of osteoclast regulatory factors c-Fos and NFATc1 by inhibiting the activation of MAPK and NF-κB pathways, and thereby inhibiting osteoclast formation and bone resorption.
In vivo
, GMP protects mice against ovariectomy-induced bone loss by regulating the balance of major factors released in bone formation and resorption. Taken together, GMP could be a potential candidate or dietary supplement for the prevention of osteoporosis.
Gadus morhua
inhibited RANKL-induced osteoclast formation by inhibiting the activation of MAPK and NF-κB pathways and reduced the bone loss caused by estrogen deficiency in OVX-mice, showing potential anti-osteoporosis activity. |
---|---|
Bibliography: | Electronic supplementary information (ESI) available. See DOI 10.1039/d1fo03696c |
ISSN: | 2042-6496 2042-650X |
DOI: | 10.1039/d1fo03696c |