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Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway

Tingting Luo1, Xiazhou Fu1, Yaoli Liu1

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan 430000, China.

Molecules (Basel, Switzerland)
|January 15, 2021
PubMed

Insights

Sulforaphane (SFN) inhibits bone-resorbing osteoclast formation by suppressing autophagy. This study reveals autophagy as a key mechanism in SFN

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoclasts are critical cells responsible for bone resorption.
  • Osteoclast overactivity leads to bone diseases like osteoporosis.
  • Sulforaphane (SFN) shows potential in preventing osteoclastic bone destruction, but its mechanism is unclear.

Purpose of the Study:

  • To investigate the role of autophagy in sulforaphane's (SFN) anti-osteoclastogenic effects.
  • To elucidate the involvement of the JNK signaling pathway in SFN-mediated osteoclast regulation.

Main Methods:

  • Osteoclastogenesis models using RAW264.7 cells and bone marrow macrophages (BMMs) induced by RANKL.
  • Tartrate-resistant acid phosphatase (TRAP) staining for osteoclast identification.
  • Transmission electron microscopy (TEM) for autophagosome observation.
  • Western blot (WB) analysis for protein expression and phosphorylation.
  • In vivo studies using microcomputed tomography (CT), immunohistochemistry (IHC), and immunofluorescence (IF).

Main Results:

  • SFN significantly inhibited osteoclastogenesis and reduced autophagosome formation in vitro.
  • SFN suppressed the accumulation of autophagic proteins and reversed autophagy-induced osteoclastogenesis.
  • SFN inhibited JNK phosphorylation, while JNK modulation affected autophagy.
  • In vivo, SFN decreased osteoclast number, LC3 expression, and protected against LPS-induced bone erosion.

Conclusions:

  • Autophagy is a critical mechanism underlying SFN's anti-osteoclastogenic activity.
  • The JNK signaling pathway plays a role in SFN-mediated regulation of autophagy and osteoclastogenesis.
  • SFN demonstrates therapeutic potential for bone diseases characterized by excessive osteoclast activity.
Keywords:
JNK signaling pathwayautophagyosteoclastogenesissulforaphane

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