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Effects of celecoxib on human chondrocytes - enhanced production of chemokines
H. Nakamura, K. Masuko, K. Yudoh, T. Kato, K. Nishioka
CER2932
2007 Vol.25, N°1
PI 0011, PF 0016
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PMID: 17417984 [PubMed]
Abstract
OBJECTIVES:
The purpose of this study was to examine the effects of a selective cyclooxigenase-2 (COX-2) inhibitor (celecoxib) comparing diclofenac.
METHODS:
Using chondrocytes derived from cartilage of non-arthritic (NA) subjects or patients with osteoarthritis (OA) or rheumatoid arthritis (RA), we examined the effects of celecoxib on incorporation of <sup>3</sup>H-thymidine and <sup>35</sup>S-sulfate, apoptosis, and production of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, and regulated upon activation, normal T cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1a and nitric oxide (NO).
RESULTS:
Celecoxib and diclofenac tended to reduce <sup>3</sup>H-tymidine incorporation of chondrocytes. Celecoxib induced apoptosis in a dose-dependent manner, but to a lesser degree than diclofenac. Celecoxib inhibited proteoglycan synthesis (indicated by <sup>35</sup>S-sulfate incorporation) in NA chondrocytes, but not in OA and RA chondrocytes. Celecoxib increased interleukin-1 (IL-1)-induced production of RANTES and MIP-1α by chondrocytes and decreased IL-1-induced NO production by chondrocytes, whereas it did not affect MMP production.
CONCLUSIONS:
Celecoxib had both beneficial and adverse effects on chondrocytes. RA, OA and NA chondrocytes showed different responses. Interestingly, celecoxib enhanced the production of chemokines.
