Vitexin suppresses RANKL-induced osteoclastogenesis and prevents lipopolysaccharide (LPS)-induced osteolysis.
J Cell Physiol
; 234(10): 17549-17560, 2019 08.
Article
en En
| MEDLINE
| ID: mdl-30793311
ABSTRACT
Osteolytic diseases are characterized by an increase in the number and/or activity of bone-resorbing osteoclasts. Identification of natural compounds that can suppress osteoclast formation and function is crucial for the prevention and treatment of osteolytic diseases. Vitexin, a naturally-derived flavonoid extracted from various medicinal plant species, demonstrates a broad range of pharmacological properties including anticancer and anti-inflammatory effects. Here in this study, we showed that vitexin exerts antiosteoclastogenic effects by directly inhibiting receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation and bone resorption in vitro and protected against lipopolysaccharide (LPS)-induced inflammatory osteolysis in vivo. Vitexin suppressed the early activation of ERK and p38 MAPK pathways in response to RANKL thereby attenuating the downstream induction of c-Fos and NFATc1, and abrogating the expression of osteoclast marker genes. Collectively, these results provide evidence for the therapeutic application of vitexin in the treatment of osteoclast-mediated bone lytic diseases.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Osteogénesis
/
Osteólisis
/
Apigenina
/
Ligando RANK
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Año:
2019
Tipo del documento:
Article