Alginate Oligosaccharide prevents and treats diseases related to inflammation, oxidative stress and immunity. This study evaluated the effect of AOS on osteoporosis and explored its mechanism of action. The osteoporosis model was induced with d-galactose (d-gal) (200 mg·kg-1·d-1) for 8 weeks. Mice in three groups were given AOS (50, 100, 150 mg·kg-1·d-1) by gavage for 4 weeks, and the control group was given sterile water (5 mL·kg-1·d-1) by gavage for 8 weeks. The results showed that AOS improved bone mineral density and bone microstructure in d-gal-induced osteoporotic mice. AOS may inhibit osteoclast proliferation by inhibiting receptor activator of nuclear factor-kB ligand (RANKL)-kB (NF-kB)-related nuclear factor-kB (NF-kB) and c-Fos signaling pathways. In senile osteoporosis, AOS also increased the expression of osteoprotegerin (OPG) and competitively inhibited the binding between RANK and RANKL. In addition, AOS decreased serum osteocalcin secretion and reduced bone turnover. The results demonstrated the anti-osteoporosis effect of AOS on osteoporotic mice.
Note: The Alginate Oligosaccharide used in this experiment was provided by our company, Qingdao BZ Oligo Biotech Co., Ltd.
From "Alginate oligosaccharide alleviates senile osteoporosis via the RANKL-RANK pathway in D-galactose-induced C57BL/6J mice."
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