Asiatic Acid Inhibits OVX-Induced Osteoporosis and Osteoclastogenesis Via Regulating RANKL-Mediated NF-κb and Nfatc1 Signaling Pathways
is a triterpenoid compound extracted from a medicinal plant . It has been used as a highly efficient compound for the treatment of cancer and hyperlipidemia, as well as possessing potential antiinflammatory properties. However, its effects on bone metabolism and osteoporosis haven't been report...
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Veröffentlicht in: | Frontiers in pharmacology 2020-03, Vol.11, p.331-331 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | is a triterpenoid compound extracted from a medicinal plant
. It has been used as a highly efficient compound for the treatment of cancer and hyperlipidemia, as well as possessing potential antiinflammatory properties. However, its effects on bone metabolism and osteoporosis haven't been reported. The purpose of our research were to reveal the biomolecular effects of
on osteoclasts, and its underlying molecular mechanisms regulating its effects on receptor activator of NF-κB ligand (RANKL)-induced signaling pathways. We found that
inhibited multinucleated tartrate-resistant acid phosphatase (TRAcP)-positive osteoclast differentiation and osteoclast induced bone loss. Real time PCR showed that
reduced the expression of down-cascade target genes including
,
,
, and
. Western blot and luciferase reporter gene assays revealed that
inhibits RANKL mediated NF-κB and NFATc1 signalings. Further,
study demonstrated
attenuates estrogen deficiency-induced bone loss in ovariectomized mice. MicroCT and histology analyses revealed that osteoclast numbers were significantly suppressed in
treated groups. Furthermore, serum levels of TRAcP and CTX-1 were downregulated in treated groups. Taken together, our data show that
can inhibit osteoclastic formation and reduce OVX-induced bone resorption through RANKL-activated NF-κB or NFATc1 signaling, suggesting that
may be a potential and effective natural compound for the therapy of excessive RANKL-related osteolytic diseases. |
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ISSN: | 1663-9812 1663-9812 |
DOI: | 10.3389/fphar.2020.00331 |