Effect of triptolide on expression of receptor activator of nuclear factor-κB ligand in rat adjuvant induced arthritis

@article{Yonghong2008EffectOT,
  title={Effect of triptolide on expression of receptor activator of nuclear factor-$\kappa$B ligand in rat adjuvant induced arthritis},
  author={Huang Yonghong and Luo Bo and Zhang Mingmin and Tu Sheng-hao and Zeng Keqing},
  journal={Journal of Huazhong University of Science and Technology [Medical Sciences]},
  year={2008},
  volume={26},
  pages={344-346}
}
  • H. Yonghong, L. Bo, +2 authors Zeng Keqing
  • Published 2008
  • Medicine
  • Journal of Huazhong University of Science and Technology [Medical Sciences]
SummaryThe effect of triptolide (TP) on the expression of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) was explored in rat adjuvant induced arthritis (AA). AA was induced in Wistar rats. Arthritis rats were treated with TP and methotrexate (MTX) at the onset (day 9) of arthritis. On the peak of arthritis (day 24), the expression of RANKL and OPG protein in the joints and RANKL mRNA in peripheral blood mononuclear cells (PBMC) was detected. TNF-α and IL-1… Expand
Cardiotrophin-1 Induces Tumor Necrosis Factor α Synthesis in Human Peripheral Blood Mononuclear Cells
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A new mechanism for elevated serum TNFα concentrations and PBMC activation in CHF is revealed besides the hypothesis ofPBMC activation by bacterial translocation from the gut, indicating that NFκB seems to be necessary. Expand
Triptolide inhibits osteoclast formation, bone resorption, RANKL-mediated NF-қB activation and titanium particle-induced osteolysis in a mouse model
  • Jianbin Huang, Lin Zhou, +13 authors Yue Ding
  • Chemistry, Medicine
  • Molecular and Cellular Endocrinology
  • 2015
TLDR
Triptolide inhibited osteoclastogenesis and bone resorption, as well as RANKL-induced NF-қB activities as monitored by luciferase reporter gene assays and the nuclear translocation of p65.7 cells suggest that triptolide might have therapeutic potential for the treatment of bone lytic diseases caused by prosthetic wear particles. Expand

References

SHOWING 1-9 OF 9 REFERENCES
Role for osteoprotegerin in rheumatoid inflammation.
TLDR
The possibility that OPG therapy to block this mechanism might prove beneficial in patients with RA is raised, which raises the possibility that the bony erosions seen in RA may result from RANKL/RANK system activation by activated T cells. Expand
Osteoprotegerin (OPG) acts as an endogenous decoy receptor in tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL)‐mediated apoptosis of fibroblast‐like synovial cells
TLDR
OPG is an endogenous decoy receptor for TRAIL‐induced apoptosis of FLS, and IL‐1β seems to promote the growth of rheumatoid synovial tissues through stimulation of OPG production, which interferes with TRAIL death signals in a competitive manner. Expand
Interleukin (IL) 18 stimulates osteoclast formation through synovial T cells in rheumatoid arthritis: comparison with IL1β and tumour necrosis factor α
TLDR
IL18, IL1β, or TNFα can indirectly stimulate osteoclast formation through up regulation of RANKL production from T cells in RA synovitis; IL18 is as effective as IL1 β, but less potent than TNF α. Expand
Interleukin (IL) 18 stimulates osteoclast formation through synovial T cells in rheumatoid arthritis: comparison with IL1 beta and tumour necrosis factor alpha.
TLDR
IL18, IL1 beta, or TNF alpha can indirectly stimulate osteoclast formation through up regulation of RANKL production from T cells in RA synovitis; IL18 is as effective as IL1 Beta, but less potent than TNFalpha. Expand
Duration of bone protection by a single osteoprotegerin injection in rats with adjuvant-induced arthritis
TLDR
It is indicated that one OPG injection will inhibit joint erosions for several days, and confirmed that bone-sparing therapy must be initiated early in disease to protect joint integrity. Expand
Experimental investigation on triptolide induced apoptosis of synoviocytes in collagen induced arthritis rat
TLDR
Triptolide can induce apoptosis of synoviocytes in CIA rats and may be one of the mechanisms of triptolide in treating rheumatoid arthritis. Expand
Osteoclastic activation is the principal mechanism leading to secondary osteoporosis in rheumatoid arthritis.
TLDR
This study suggests that osteoclastic activation, rather than suppression of bone formation, is the dominant process leading to bone loss in early RA and provides a rational approach for selecting and treating patients with RA to reduce their established longterm risk of osteoporotic fracture. Expand
Pathogenesis of bone erosions in rheumatoid arthritis.
TLDR
Analysis of RA synovium and joint tissues from animal models of inflammatory arthritis, as well as cell and tissues culture studies, have helped to define the cytokines and inflammatory mediators that are involved in the recruitment and activation of bone resorbing cells associated with focal bone erosions. Expand
Osteoporosis in Rheumatoid Arthritis
TLDR
Strong support is given to Havens's original conclusion that haemagglutinating activity revealed by the sera of some patients with infective hepatitis is not due to the causative virus but is a manifestation of one of the serum changes associated with hepatic dysfunction. Expand