Diallyl disulfide alleviates inflammatory osteolysis by suppressing osteoclastogenesis via NF-κB-NFATc1 signal pathway

FASEB J. 2019 Jun;33(6):7261-7273. doi: 10.1096/fj.201802172R. Epub 2019 Mar 11.

Abstract

Skeletal homeostasis is closely effectuated by the regulation of bone formation and bone resorption. Osteoclasts are multinuclear giant cells responsible for bone resorption. Overactivated osteoclasts and excessive bone resorption result in various lytic bone diseases, such as osteoporosis, osteoarthritis, periprosthetic infection, and inflammatory aseptic loosening of orthopedic implants. In consideration of the severe side effects caused by the currently available drugs, exploitation of novel drugs has gradually attracted attention. Because of its anti-inflammatory, antioxidant, and antitumor capacities, diallyl disulfide (DADS), a major oil-soluble organosulfur ingredient compound derived from garlic, has been widely researched. However, the effects of DADS on osteoclasts and lytic bone diseases are still unknown. In this study, we investigated the effects of DADS on receptor activator of NF-κB ligand (RANKL)- and LPS-mediated osteoclastogenesis, LPS-stimulated proinflammatory cytokines related to osteoclasts, and LPS-induced inflammatory osteolysis. The results showed that DADS significantly inhibited RANKL-mediated osteoclast formation, fusion, and bone resorption in a dose-dependent manner via inhibiting the NF-κB and signal transducer and activator of transcription 3 signaling and restraining the interaction of NF-κB p65 with nuclear factor of activated T cells cytoplasmic 1. Furthermore, DADS also markedly suppressed LPS-induced osteoclastogenesis and reduced the production of proinflammatory cytokines with LPS stimulation to indirectly mediate osteoclast formation. Consistent with the in vitro results, DADS prevented the LPS-induced severe bone loss by blocking the osteoclastogenesis. All of the results indicate that DADS may be a potential and exploitable drug used for preventing and impeding osteolytic lesions.-Yang, J., Tang, R., Yi, J., Chen, Y., Li, X., Yu, T., Fei, J. Diallyl disulfide alleviates inflammatory osteolysis by suppressing osteoclastogenesis via NF-κB-NFATc1 signal pathway.

Keywords: bone resorption; natural products; osteoclast.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allyl Compounds / pharmacology*
  • Allyl Compounds / therapeutic use
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Bone Resorption / drug therapy
  • Cell Differentiation / drug effects
  • Disulfides / pharmacology*
  • Disulfides / therapeutic use
  • Endotoxemia / complications
  • Female
  • Inflammation
  • Lipopolysaccharides / toxicity
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Macrophages / cytology
  • Macrophages / drug effects
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / physiology*
  • Osteoclasts / drug effects*
  • Osteoclasts / pathology
  • Osteolysis / drug therapy*
  • Osteolysis / etiology
  • RANK Ligand / antagonists & inhibitors
  • RANK Ligand / pharmacology
  • RAW 264.7 Cells
  • Random Allocation
  • Recombinant Proteins / pharmacology
  • STAT3 Transcription Factor / antagonists & inhibitors
  • STAT3 Transcription Factor / physiology
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology

Substances

  • Allyl Compounds
  • Anti-Inflammatory Agents
  • Disulfides
  • Lipopolysaccharides
  • NF-kappa B
  • RANK Ligand
  • Recombinant Proteins
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tnfsf11 protein, mouse
  • diallyl disulfide
  • Macrophage Colony-Stimulating Factor