This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
Research
Lingling Zhou
Nanjing University of Chinese Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9564-0902
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Bone erosion is an important problem in rheumatoid arthritis (RA). The role of osteoclast in bone resorption is critical in RA, and intervention of osteoclast differentiation can improve bone destruction. Tripterygium wilfordii Hook F (TW) can improve the symptoms of RA. The effect of triptolide (TP), which is a purified component of TW, on bone destruction in RA and its mechanism remain unclear.
Methods: We investigated the effect of TP on osteoclast differentiation using a co-culture system of synovial fibroblasts and monocytes from adjuvant-induced arthritic rats. We also investigated the effect of TP on murine collagen-induced arthritis (CIA).
Results: The results showed that a certain dose of TP inhibited the differentiation of osteoclast, and reduced the levels of interleukin (IL)-1, IL-34, macrophage colony stimulating factor (M-CSF), receptor activator for nuclear factor-κ B Ligand (RANKL), and osteopontin (OPN) in the co-culture supernatant of synovial fibroblasts and monocytes. Furthermore, a certain dose of TP reduced the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6), mitogen-activated protein kinases (MAPKs) and nuclear factor of activated T cells 1 (NFATc1) in osteoclast. Meanwhile, TP reduced the symptoms of arthritis and bone destruction in CIA.
Conclusion: Our results suggest that TP can improve the bone destruction of murine arthritis, and the mechanism is related to the inhibition of osteoclast differentiation via TRAF6/MAPKs/NFATc1 signaling pathway.
Keywords
triptolide, osteoclast, RANKL, TRAF6, MAPK, NFATc1
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 07 Apr, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Internal Medicine
Learn more about our company.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Lingling Zhou
Nanjing University of Chinese Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9564-0902
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 07 Apr, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Internal Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Bone erosion is an important problem in rheumatoid arthritis (RA). The role of osteoclast in bone resorption is critical in RA, and intervention of osteoclast differentiation can improve bone destruction. Tripterygium wilfordii Hook F (TW) can improve the symptoms of RA. The effect of triptolide (TP), which is a purified component of TW, on bone destruction in RA and its mechanism remain unclear.
Methods: We investigated the effect of TP on osteoclast differentiation using a co-culture system of synovial fibroblasts and monocytes from adjuvant-induced arthritic rats. We also investigated the effect of TP on murine collagen-induced arthritis (CIA).
Results: The results showed that a certain dose of TP inhibited the differentiation of osteoclast, and reduced the levels of interleukin (IL)-1, IL-34, macrophage colony stimulating factor (M-CSF), receptor activator for nuclear factor-κ B Ligand (RANKL), and osteopontin (OPN) in the co-culture supernatant of synovial fibroblasts and monocytes. Furthermore, a certain dose of TP reduced the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6), mitogen-activated protein kinases (MAPKs) and nuclear factor of activated T cells 1 (NFATc1) in osteoclast. Meanwhile, TP reduced the symptoms of arthritis and bone destruction in CIA.
Conclusion: Our results suggest that TP can improve the bone destruction of murine arthritis, and the mechanism is related to the inhibition of osteoclast differentiation via TRAF6/MAPKs/NFATc1 signaling pathway.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Loading...