Effects of triptolide on cell proliferation and regulation of Ras-MAPKs pathway in synoviocytes induced by tumor necrosis factor.
- Author:
Jianzhu WANG
1
;
Jinrao LIAN
;
Xiangying KONG
;
Na LIN
Author Information
- Publication Type:Journal Article
- MeSH: 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; drug effects; metabolism; Tumor Necrosis Factor-alpha; pharmacology; ras Proteins; metabolism
- From: China Journal of Chinese Materia Medica 2010;35(7):888-891
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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).
METHODRA-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.
RESULTTriptolide 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.
CONCLUSIONTriptolide 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.
