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Rosiglitazone inhibits osteoclastogenesis in rheumatoid arthritis by down-regulating RANKL expression and suppressing ERK phosphorylation / 中国病理生理杂志
Article in Zh | WPRIM | ID: wpr-464259
Responsible library: WPRO
ABSTRACT

AIM:

To investigate the effects of rosiglitazone on fibroblast-like synoviocyte ( FLS )-induced osteoclastogenesis in rheumatoid arthritis ( RA) and the related mechanism.

METHODS:

RA-FLS were cocultured with peripheral blood monocytes from healthy volunteers in the presence of macrophage colony-stimulating factor ( M-CSF) and rosiglitazone.Osteoclasts were assayed by tartrate-resistant acid phosphatase ( TRAP) staining.Resorption lacunae area was identified by toluidine blue staining and quantified by image analysis software.The mRNA expression of RANKL and OPG was evaluated by real-time PCR, and the protein levels of RANKL, OPG, p-ERK, p-p38 and p-JNK were measured by Western blot.

RESULTS:

Compared with control group ( without rosiglitazone treatment) , rosiglitazone at concentration of 15 μmol/L significantly decreased the number of osteoclasts (P0.05 ) .

CONCLUSION:

Rosiglitazone inhibits RA-FLS-induced osteoclast formation and its resorption activity by down-regulating RANKL expression and ERK phosphorylation, suggesting that rosiglitazone may inhibit RA osteoclastogenesis and bone re-sorption.
Key words
Full text: 1 Index: WPRIM Type of study: Prognostic_studies Language: Zh Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article
Full text: 1 Index: WPRIM Type of study: Prognostic_studies Language: Zh Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article