J Bone Metab.  2020 Feb;27(1):53-63. 10.11005/jbm.2020.27.1.53.

Inhibitory Effect of Rosae Multiflorae Fructus Extracts on the Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis through Modulation of P38- and Ca2⁺-Mediated Nuclear Factor of Activated T-Cells Cytoplasmic 1 Expression

Affiliations
  • 1Department of Oral Microbiology and Immunology, College of Dentistry, Wonkwang University, Iksan, Korea. leesh2@wku.ac.kr
  • 2Department of Oral Physiology, College of Dentistry, Wonkwang University, Iksan, Korea.
  • 3Institute of Biomaterials and Implant, College of Dentistry, Wonkwang University, Iksan, Korea.

Abstract

BACKGROUND
Rosae Multiflorae fructus (RMF), known to have anti-inflammatory and antioxidant properties, has been used as a traditional remedy for inflammatory diseases such as arthritis in Eastern Asia. However, its effect on osteoclasts, which play a crucial role in resorptive inflammatory bone diseases, is yet to be elucidated.
METHODS
The effect of extract of RMF (RMF-E) on receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis was examined by tartrate-resistant acid phosphatase (TRAP) staining, real-time polymerase chain reaction and western blot analysis. In addition, RANKL-induced Ca2⁺-oscillation was also investigated.
RESULTS
RMF-E remarkably inhibited TRAP+-osteoclast and resorptive pit formation in a dose-dependent manner. In addition, the expression of c-Fos and nuclear factor of activated T-cells cytoplasmic, known as pivotal transcription factors for osteoclast formation in vitro and in vivo, and that of the osteoclast differentiation markers such as Acp5, Oscar, CtsK, Atp6v0d2, Tm7sf4, and Nfatc1 were significantly decreased by RMF-E treatment during osteoclastogenesis. The inhibitory effect of RMF-E on RANKL-induced osteoclastogenesis was caused by the suppression of p38 mitogen-activated protein kinase activation, and RANKL-induced Ca2⁺-oscillation removal via inactivation of Bruton's tyrosine kinase (BTK), and subsequently phospholipase C-γ2.
CONCLUSIONS
RMF-E negatively regulates osteoclast differentiation and formation. These findings suggest the possibility of RMF-E as a traditional therapeutic agent against osteoclast-related bone disorders such as osteoporosis, rheumatoid arthritis, and periodontitis.

Keyword

Osteoclasts; Bone diseases; NFATc1; Calcium signaling; Osteogenesis

MeSH Terms

Acid Phosphatase
Antigens, Differentiation
Arthritis
Arthritis, Rheumatoid
Blotting, Western
Bone Diseases
Calcium Signaling
Cytoplasm*
Far East
In Vitro Techniques
Osteoclasts
Osteogenesis
Osteoporosis
Periodontitis
Phospholipases
Protein Kinases
Protein-Tyrosine Kinases
Real-Time Polymerase Chain Reaction
Rosa*
T-Lymphocytes*
Transcription Factors
Acid Phosphatase
Antigens, Differentiation
Phospholipases
Protein Kinases
Protein-Tyrosine Kinases
Transcription Factors
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