GAG and collagen II attenuate glucocorticoid-induced osteoporosis by regulating NF- κB and MAPK signaling.

In this study, we aimed to determine the concrete effect and the mechanism of GAG and collagen II on glucocorticoid-induced osteoporosis. We implanted prednisolone pellets subcutaneously in mice to mimic glucocorticoid-induced osteoporosis. GAG was administered intragastrically every day for 60 days. The results demonstrated a protective effect of GAG and collagen II on glucocorticoid-induced osteoporosis. Trabecular number and connection density increased after treatment with GAG and collagen II. We generated bone marrow-derived macrophages to explore the effect of GAG and collagen II on osteoclast differentiation. We collected cell protein and RNA in the presence of macrophage colony-stimulating factor (M-CSF) and receptor activator for nuclear factor-κB ligand (RANKL) and found that GAG and collagen II inhibited the NF-κB and MAPK pathways, thereby down-regulating osteoclast differentiation molecules such as matrix metallopeptidase 9 (MMP 9) and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc-1). Our findings suggest that GAG and collagen II may have therapeutic potential of patients with glucocorticoid-induced osteoporosis in clinical settings. PMID: 30018717 [PubMed]
Source: American Journal of Translational Research - Category: Research Tags: Am J Transl Res Source Type: research