[Effects of triptolide on cell proliferation and regulation of Ras-MAPKs pathway in synoviocytes induced by tumor necrosis factor]

Zhongguo Zhong Yao Za Zhi. 2010 Apr;35(7):888-91. doi: 10.4268/cjcmm20100719.
[Article in Chinese]

Abstract

Objective: To investigate the effects of triptolide on proliferation and regulation of ras-MAPKs pathway in human fibroblast-like synoviocytes of rheumatoid arthritis (RA-HFLS) treated with tumor necrosis factor (TNF-alpha).

Method: RA-HFLS were cultured with TNF-alpha in the presence or absence of variable doses of triptolide (0.28, 2.8, 28, 140 nmol x L(-1)) in vitro. Cell proliferation was evaluated by MTS assay. The phosphorylation status of Ras-MAPKs-associated proteins (Ras, p-P38, p-ERK and p-JNK) were detected by Western blot analysis.

Result: Triptolide could obviously decrease the RA-HFLS viability in a dose-dependent manner and the inhibition ratio was 0.28%, 5.05%, 30.83% and 43.77% respectively. In addition, triptolide could also suppressed the expression of Ras, p-P38, p-ERK and p-JNK.

Conclusion: Triptolide has an notable inhibiting effect on proliferation of RA-HFLS and the molecule mechanism is due in part to the direct suppression of abnormal activation of Ras-MAPKs pathway.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Cell Line
  • Cell Proliferation / drug effects
  • Diterpenes / pharmacology*
  • Epoxy Compounds / pharmacology
  • Gene Expression Regulation / drug effects
  • MAP Kinase Signaling System / drug effects*
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism*
  • Phenanthrenes / pharmacology*
  • Synovial Membrane / cytology*
  • Synovial Membrane / drug effects*
  • Synovial Membrane / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*
  • ras Proteins / metabolism*

Substances

  • Diterpenes
  • Epoxy Compounds
  • Phenanthrenes
  • Tumor Necrosis Factor-alpha
  • triptolide
  • Mitogen-Activated Protein Kinases
  • ras Proteins